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1
Daja, Mirella Maria. "Enzyme activities associated with gonadotropic hormones." Thesis, University of Auckland, 1993. http://hdl.handle.net/2292/2311.
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A structural relationship between gonadotropic hormones and certain types of enzymes has been suggested in previous studies and an investigation into the possibility of enzymatic activity associated with the gonadotropic hormones has been the primary focus of the research presented in this thesis. Partial sequence homology between human chorionic gonadotropin (hCG) and α-chymotrypsin prompted the recent proposal of a tertiary structure of hCG using α-chymotrypsin as a folding template, which suggested the possibility of intrinsic peptidase activity associated with hCG. Highly purified hCG (CR127) was assayed for enzymatic activity against a range of synthetic peptide substrates and was found to exhibit Arg-specific peptidase activity. This activity was almost completely inhibited by diisopropylfluorophosphate (DFP), soybean trypsin inhibitor (STI), N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and to a lesser extent by N-α-p-tosyl-L-lysine chloromethyl ketone (TLCK), which indicated that the observed protease activity was serine protease-like. To establish whether this activity was intrinsic to the hormone or due to contaminants, extensive purification procedures were carried out. Hydrophobic interaction chromatography (HIC) and soybean trypsin inhibitor-affinity chromatography were found to effectively separate the protease activity from the hormone, indicating the presence of exogenous protease contaminants in the highly purified preparation of hCG. Further analysis by [3H]-DFP labelling of hCG and SDS-PAGE of the isolated contaminants revealed the presence of possible serine proteases with apparent molecular masses of 60 and 20 kD. Because serine proteases are known to stimulate cAMP production in the same target cells, it was necessary to determine the effects of the contaminating proteases on the receptor binding of hCG and cAMP production. The presence of these contaminants was found to have no apparent effect on the receptor binding capability of hCG, however the in vitro biological activity of hCG as determined by maximal cAMP production was decreased after HIC-HPLC purification of the hormone. These observations suggested that the serine protease-like contaminants contributed to the total cAMP production, thereby introducing significant error in biological assays that use hCG (CR127). The possible intrinsic enzymatic activity of hCG against its receptor as a natural substrate was further investigated. A membrane-bound receptor preparation was isolated from porcine ovaries and a receptor binding assay successfully established. The effects of hCG binding upon the membrane-bound receptor were studied and receptor proteolysis was observed. However, this proteolysis could not be definitively attributed to the actions of hCG. A purified receptor was subsequently prepared by hCG-affinity chromatography and analysed by SDS-PAGE with detection by autoradiography and silver staining. The purified receptor was found to have undergone proteolysis during the purification procedure, presumably following incubation with the hCG affinity matrix. Recent reports of the presence of homologous amino acid sequences in the active site of thioredoxin and the β-subunit of the gonadotropic hormones luteinizing hormone (LH) and follicle stimulating hormone (FSH), and subsequent demonstration of thioredoxin-like activity associated with these hormones, prompted an investigation into the possibility of thioredoxin-like activity associated with hCG. LH, FSH and hCG were all assayed for their ability to promote reactivation of reduced and denatured RNase. Although LH was shown to be capable of reactivating reduced RNase, the level of activity detected was significantly lower than that previously reported, whereas FSH and hCG were not found to be capable of this thioredoxin-like activity. These results suggested that the previously reported thioredoxin-like activity may be due to contamination of the hormone preparation, by the ubiquitous enzyme thioredoxin. The possibility of LH possessing intrinsic dithiol-disulphide interchange activity was investigated further using [3H]-iodoacetic acid. RNase/LH were incubated in an attempt to quench a dithiol intermediate. Preliminary results suggested that the presence of LH in this reaction increased the amount of protein radiolabelled, however, the isolation of a radiolabelled dithiol intermediate which could be conclusively identified as LH was not forthcoming. Furthermore the lack of RNase reactivation activity in hCG, suggests that the putative thioredoxin-like activity of LH, if intrinsic, may not be involved in receptor activation and/or signal transduction, as hCG and LH share the same receptor and should therefore have a similar mechanism of activation.
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Silva, Laura Arnt. "Maturação e fertilização in vitro de oócitos estádio III de zebrafish." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/140108.
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Protocolos de sucesso para a maturação in vitro de oócitos de peixe são importantes, uma vez que é necessário para garantir uma fertilização bem sucedida, formação do zigoto, crescimento do embrião e seu completo desenvolvimento. Em algumas espécies, a eficiência deste processo ainda é muito baixa ou restrita a poucas substâncias que podem ser utilizadas. Assim, pesquisou-se a utilização de hormônios alternativos ao protocolo já existente para maturação in vitro de ovócitos de zebrafish. O objetivo foi avaliar a eficiência do extrato de hipófise de carpa (EHC), dos hormônios folículo estimulante (FSH) e luteinizante (LH) para fazer a maturação dos ovócitos estádio III de zebrafish. Os oócitos estádio III foram colocados em meio de cultivo Leibovitz modificado, suplementado com soro fetal bovino e adicionado o hormônio correspondente a seu tratamento (T1-controle; T2-16 μg/ml de EHC; T3- 32 μg/ml de EHC; T4- 48 μg/ml de EHC; T5- 64 μg/ml de EHC; T6- 80 μg/ml de EHC; T7- 0,5 μg/ml de FSH; T8- 0,5 μg/ml de LH e T9- 0,5 μg/ml de FSH e 0,5 μg/ml de LH). A taxa de maturação foi avaliada através da visualização da quebra da vesícula germinal (GVBD). Em todos os tratamentos houve maturação, embora o EHC tenha demonstrado taxas de maturação muito baixas (T2= 12,8%; T3=24,8%; T4=27%; T5=22,7%; T6=9,7%) e inferiores em relação a maior eficiência dos hormônios gonadotrópicos (T7=16%; T8=35%; T9=50%). Além disso foi possível verificar a viabilidade dos oócito através da fertilização in vitro do melhor tratamento (T9) com uma taxa de eclosão e desenvolvimento em larva de 60%. Os resultados da maturação in vitro utilizando estes indutores hormonais em oócitos estádio III de zebrafish mostraram-se promissores, e reforçam as perspectivas para o aprimoramento e uso desta técnica para produção in vitro de embriões viáveis.Successful protocols for maturation of oocytes are important, as it is necessary for ensuring successful fertilization, zygote formation, embryo growth and full development. In some species the efficiency of in vitro maturation is still very low or is still restricted to a little amount of substances which can be used for the matter. Thus, we studied the use of alternative hormones to the existing protocol for in vitro maturation of zebrafish oocytes. The aim of this study was to evaluate the efficiency of the use of carp pituitary extract (CPE), the follicle stimulating hormone (FSH) and luteinizing hormone (LH) to oocyte maturation stage III of zebrafish. Oocytes stage III were placed in modified Leibovitz culture medium, suplemented with fetal bovine serum and added to the correnponding hormone treatment (T1-control; T2-16 g / ml of CHE; T3 32 g / ml of CHE, T4 - 48 g / ml of CHE; T5- 64 g / ml of CHE; T6- 80 g / ml of CHE; T7- 0.5 g / ml of FSH, T8 0.5 mg / ml of LH and T9- 0.5 g / ml of FSH and 0.5 mg / ml LH). The maturation rate was assessed by the germinal vesicle break down (GVBD). In all cases there was maturation, though the EHC has demonstrated fairly low maturation rate (T2= 12,8%; T3=24,8%; T4=27%; T5=22,7%; T6=9,7%) and lower in relation of the high efficiency presented by the gonadotropic hormones (T7=16%; T8=35%; T9=50%). In addition it was possible to verify the viability of the oocyte through IVF of the best treatment (T9) with a result of 60% of hatching and larvae development rate. The results of maturation in turn using this hormones in stage III oocytes of zebrafish proved promising, and enhance the prospects for improvement and use of this technique for in vitro production of viable embryos.
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Traverse, Bastien Roger Marcel. "Activité cérébrale du système opioïde chez les sportifs d'endurance et l'anorexie mentale : Etudes TEP à la [11C]-diprénorphine." Thesis, Lyon, 2020. http://www.theses.fr/2020LYSES003.
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Le travail présenté dans cette thèse s’attache à démontrer le rôle central joué par le système opioïde dans le développement et le maintien de deux modèles d’addictions comportementales : l’anorexie mentale et l’addiction au sport.Il présente une approche originale, multidisciplinaire et transverse utilisant des techniques modernes et novatrices, avec pour procédé central une imagerie cérébrale TEP/TDM utilisant de la [11C]-diprénorphine comme traceur. Cherchant à obtenir une imagerie en densité de récepteurs opioïdes, une modélisation SRTM a été utilisée. Les images en densité de récepteurs ainsi obtenues ont été exploitées par analyse voxel à voxel sous SPM12. Ces comparaisons statistiques paramétriques ont également intégré plusieurs variables, covariables et paramètres de régressions issus d’analyses complémentaires (tests psychométriques, mesures anthropométriques et analyses biologiques, notamment des dosages d’opioïdes en circulation périphérique mesurés par une technique ELISA).Ces analyses ont démontré la complexité du mécanisme addictif dans ces deux modèles, avec un rôle indirect du système opioïde probablement par modulation du circuit dopaminergique de la boucle méso limbique du circuit de la récompense. Cependant les nombreuses divergences entre ces deux addictions comportementales et les hétérogénéités retrouvées entre les individus montre aussi l’existence d’une sensibilité et de mécanismes variables d’une personne à l’autre, posant la question du phénotypage et de la génétique, et ouvrant le champ à de nouvelles études, avec à terme de possibles répercussions cliniques voire thérapeutiquesThis thesis aims to demonstrate the central role of opioid system in developing and maintaining addiction in two behavioural addiction models: sport addiction and anorexia nervosa.It presents an original, multidisciplinary and transversal approach using modern and innovative tools, with a brain imagery using [11C]-diprenorphine PET-scan as main process. We attempt to get receptor density mapping using a SRTM model. Images obtained by this way were then exploited by voxel-based analysis using SPM12. Statistical parametric comparisons include several variables, covariables and regression parameters extracted from complementary exams (psychometric tests, anthropometric measurements, biological samplings especially peripheric circulating opioids assessment by ELISA technic).These analyses demonstrate the complexity of addictive mechanisms in these two models, with an indirect role of opioid system which seems to work by modulation of dopaminergic mesolimbic reward system. However, we also find several differences and inhomogeneities in these two behavioural addictions which indicate existence of various sensitivity and different mechanisms among subjects. This asks the question of phenotyping and genetics underlying these phenomena, needing new studies with a long-term perspective of clinical and therapeutic possibilities
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Sadie, Hanél. "Transcriptional regulation of the mouse gonadotropin-releasing hormone receptor gene in pituitary gonadotrope cell lines." Thesis, Stellenbosch : University of Stellenbosch, 2006. http://hdl.handle.net/10019.1/1495.
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Thesis (PhD (Biochemistry))--University of Stellenbosch, 2006.Gonadotropin-releasing hormone (GnRH), acting via its cognate receptor (GnRHR) is the primary regulator of mammalian reproductive function. Pituitary sensitivity to GnRH can be directly correlated with GnRHR levels on the surface of the pituitary gonadotrope cells, which can be regulated at transcriptional, post-transcriptional and post-translational levels. This study investigated mechanisms of transcriptional regulation of mouse GnRHR expression in two mouse gonadotrope cell lines, αT3-1 and LβT2, using a combination of endogenous mRNA expression studies, promoter-reporter studies, a two-hybrid protein-protein interaction assay, Western blotting, and in vitro protein-DNA binding studies. In the first part of the study, the role of two GnRHR promoter nuclear receptor binding sites (NRSs) and their cognate transcription factors in basal and Protein Kinase A (PKA)-stimulated regulation of GnRHR promoter activity was investigated in αT3-1 cells. The distal NRS was found to be crucial for basal promoter activity in these cells. While the NRSs were not required for the PKA response in these cells, results indicate a modulatory role for the transcription factors Steroidogenic Factor-1 (SF-1) and Nur77 via these promoter elements. The second part of the study focused on elucidating the mechanism of homologous regulation of GnRHR transcription in LβT2 cells, with a view to defining the respective roles of PKA and Protein Kinase C (PKC) in the transcriptional response to GnRH. In addition, the respective roles of the NRSs, the cyclic AMP response element (CRE) and the Activator Protein-1 (AP-1) promoter cis elements, together with their cognate transcription factors, in basal and GnRH-stimulated GnRHR promoter activity, were investigated. Homologous upregulation of transcription of the endogenous gene was confirmed, and was quantified by means of real-time RTPCR. The GnRH response of the endogenous gene and of the transfected promoter-reporter construct required PKA and PKC activity, and the GnRH response of the promoter-reporter construct was found to be dependent on a functional AP-1 site. Furthermore, GnRH treatment resulted in increased binding of phosphorylated cAMP-response element binding protein (phospho-CREB) and decreased expression and binding of SF-1 to their cognate cis elements in vitro, and stimulated a direct interaction between SF-1 and CREB, suggesting that these events are also required for the full transcriptional response to GnRH. This study is the first providing detail regarding the mechanism of transcriptional regulation of GnRHR expression in LβT2 cells by GnRH. Based on results from this study, a model has been proposed which outlines for the first time the kinase pathways, the promoter cis elements and the cognate transcription factors involved in homologous regulation of GnRHR transcription in the LβT2 cell line. As certain aspects of this model have been confirmed for the endogenous GnRHR gene, the model is likely to be physiologically relevant, and provides new ideas and hypotheses to be tested in future studies.
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Corchuelo, Chavarro Sheryll Yohana [UNESP]. "GnRH/GnIH e seus receptores no sistema olfato-retinal de zebrafish." Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/134047.
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O hormônio liberador de gonadotropina (GnRH) é um dos fatores chaves na regulação neuroendócrina da reprodução dos vertebrados. Alguns peixes apresentam três variantes do GnRH: o GnRH1 envolvido na secreção de gonadotropinas, o GnRH2 que regula o comportamento alimentar e sexual e o GnRH3 expresso no bulbo olfatório e o nervo terminal cujas fibras nervosas inervam a retina e o epitélio olfatório. O zebrafish possui duas variantes do GnRH (GnRH2 e GnRH3), sendo o GnRH3 a variante hipofisiotrófica. Estudos mostram possível envolvimento do GnRH no sistema olfato-retinal. No sistema olfatório o GnRH regula a sensibilidade na detecção de alimento, o reconhecimento intra e interespecífico, entre outros. Na retina, o GnRH3 pode estar envolvido na acuidade visual e do processamento de informação da retina. Existem estudos que reportam a presença de receptores de GnRH em diferentes camadas da retina, no entanto ainda não é clara a presença de receptores no epitélio olfatório. Neste contexto, no presente estudo analisamos a localização do gnrh2, gnrh3 e seus receptores (gnrhr1,2,3 e 4) e do gnih (hormônio inibidor de gonadotropinas) no epitélio olfatório, a retina e o bulbo olfatório de machos e fêmeas adultos e comparamos a expressão destes genes em fêmeas em diferentes estágios de maturação gonadal. Para tanto, o RNA total do epitélio olfatório, retina, bulbo olfatório, cérebro e gônadas foi extraído. Com base na sequência dos genes gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3 e gnrhr4, primers forward e reverse foram desenhados para RT-PCR e qPCR. Sondas para a hibridização in situ também foram construídas para verificar os sítios de expressão destas moléculas no epitélio olfatório, retina e gônadas. Imunohistoquímica com os anticorpos anti-GnRH3 (BB8 e GF6) foram realizadas para localizar a proteína do GnRH3 nos tecidos analisados. O presente estudo apresenta um panorama da expressão do sistema...
The gonadotropin releasing hormone (GnRH) is one of the key factors involved in the neuroendocrine regulation of vertebrate reproduction. Some fish species have three GnRH variants: GnRH1 involved in gonadotropin secretion, GnRH2 regulating food and sexual behaviors and the GnRH3 which is expressed in the olfactory bulb and terminal nerve whose fibers innervate the retina and the olfactory epithelium. Two GnRH variants (GnRH2 and GnRH3) are present in the zebrafish, in which GnRH3 acts as the hypophisiotrophic variant. Recent studies have been showing the role of GnRH in the olfactory-retinal system. In the olfactory system, GnRH regulates food detection, and intra and interspecific recognition. In retina, GnRH3 may be involved in visual acuity modulation and retinal processing information. Moreover, studies have reported the presence of GnRH receptors in the retina, but not yet in the zebrafish olfactory epithelium. Therefore, the current study analyzed the presence of GnRH2, GnRH3 and its receptors (GnRH-R1,2,3 and 4) and GnIH (gonadotropin inhibitory hormone) in the olfactory epithelium, olfactory bulb, retina and in gonads of adult zebrafish. We also compared the expression of these genes during the different stages of ovarian maturation in zebrafish. For that, total RNA of the olfactory epithelium, olfactory bulb, retina and gonads was extracted with the PureLink® RNA Mini Kit(Ambion®). RT-PCR and qPCR analysis were performed using forward and reverse primers for gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3, gnrhr4 for . Probes for in situ hybridization were constructed to verify the expression sites of these molecules in the olfactory epithelium, retina, and gonads. Immunohistochemistry usinganti-GnRH3 antibodies (BB8 and GF6) were performed to identify the GnRH3 protein in these tissues. The current study presents a general expression view of GnRH/GnIH and their receptors in the olfactory epithelium-olfactory bulb-retinal axis during ...
FAPESP: 2014/02481-9
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Corchuelo, Chavarro Sheryll Yohana. "GnRH/GnIH e seus receptores no sistema olfato-retinal de zebrafish /." Jaboticabal, 2015. http://hdl.handle.net/11449/134047.
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Orientador: Laura Satiko Okada NakaghiCoorientador: Rafael Henrique Nóbrega
Banca: Elisabeth Criscuolo Urbinati
Banca: Matias Pandolfi
Resumo: O hormônio liberador de gonadotropina (GnRH) é um dos fatores chaves na regulação neuroendócrina da reprodução dos vertebrados. Alguns peixes apresentam três variantes do GnRH: o GnRH1 envolvido na secreção de gonadotropinas, o GnRH2 que regula o comportamento alimentar e sexual e o GnRH3 expresso no bulbo olfatório e o nervo terminal cujas fibras nervosas inervam a retina e o epitélio olfatório. O zebrafish possui duas variantes do GnRH (GnRH2 e GnRH3), sendo o GnRH3 a variante hipofisiotrófica. Estudos mostram possível envolvimento do GnRH no sistema olfato-retinal. No sistema olfatório o GnRH regula a sensibilidade na detecção de alimento, o reconhecimento intra e interespecífico, entre outros. Na retina, o GnRH3 pode estar envolvido na acuidade visual e do processamento de informação da retina. Existem estudos que reportam a presença de receptores de GnRH em diferentes camadas da retina, no entanto ainda não é clara a presença de receptores no epitélio olfatório. Neste contexto, no presente estudo analisamos a localização do gnrh2, gnrh3 e seus receptores (gnrhr1,2,3 e 4) e do gnih (hormônio inibidor de gonadotropinas) no epitélio olfatório, a retina e o bulbo olfatório de machos e fêmeas adultos e comparamos a expressão destes genes em fêmeas em diferentes estágios de maturação gonadal. Para tanto, o RNA total do epitélio olfatório, retina, bulbo olfatório, cérebro e gônadas foi extraído. Com base na sequência dos genes gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3 e gnrhr4, primers forward e reverse foram desenhados para RT-PCR e qPCR. Sondas para a hibridização in situ também foram construídas para verificar os sítios de expressão destas moléculas no epitélio olfatório, retina e gônadas. Imunohistoquímica com os anticorpos anti-GnRH3 (BB8 e GF6) foram realizadas para localizar a proteína do GnRH3 nos tecidos analisados. O presente estudo apresenta um panorama da expressão do sistema...
Abstract: The gonadotropin releasing hormone (GnRH) is one of the key factors involved in the neuroendocrine regulation of vertebrate reproduction. Some fish species have three GnRH variants: GnRH1 involved in gonadotropin secretion, GnRH2 regulating food and sexual behaviors and the GnRH3 which is expressed in the olfactory bulb and terminal nerve whose fibers innervate the retina and the olfactory epithelium. Two GnRH variants (GnRH2 and GnRH3) are present in the zebrafish, in which GnRH3 acts as the hypophisiotrophic variant. Recent studies have been showing the role of GnRH in the olfactory-retinal system. In the olfactory system, GnRH regulates food detection, and intra and interspecific recognition. In retina, GnRH3 may be involved in visual acuity modulation and retinal processing information. Moreover, studies have reported the presence of GnRH receptors in the retina, but not yet in the zebrafish olfactory epithelium. Therefore, the current study analyzed the presence of GnRH2, GnRH3 and its receptors (GnRH-R1,2,3 and 4) and GnIH (gonadotropin inhibitory hormone) in the olfactory epithelium, olfactory bulb, retina and in gonads of adult zebrafish. We also compared the expression of these genes during the different stages of ovarian maturation in zebrafish. For that, total RNA of the olfactory epithelium, olfactory bulb, retina and gonads was extracted with the PureLink® RNA Mini Kit(Ambion®). RT-PCR and qPCR analysis were performed using forward and reverse primers for gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3, gnrhr4 for . Probes for in situ hybridization were constructed to verify the expression sites of these molecules in the olfactory epithelium, retina, and gonads. Immunohistochemistry usinganti-GnRH3 antibodies (BB8 and GF6) were performed to identify the GnRH3 protein in these tissues. The current study presents a general expression view of GnRH/GnIH and their receptors in the olfactory epithelium-olfactory bulb-retinal axis during ...
Mestre
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Kirkpatrick, Bridgette Lee 1966. "Hormonal regulation of gonadotropin releasing hormone receptor expression in the ewe." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282660.
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Endocrine regulation of expression of GnRH receptors is an important step in the control of reproduction. During the early follicular phase of the estrous cycle in the ewe, GnRH receptor expression increases in preparation for the preovulatory surge of LH. The studies described herein were designed to further elucidate the hormonal interactions controlling GnRH receptor expression. In long-term ovariectomized ewes, neither removal of progesterone, nor the presence of estradiol affected the expression of GnRH receptors. However, in ewes ovariectomized during the luteal phase of the estrous cycle and immediately implanted with progesterone and estradiol for 48 hours, low levels of estradiol for 24 hours were required to increase GnRH receptor mRNA following the removal of progesterone. In ovariectomized ewes following hypothalamic-pituitary disconnection, low levels of estradiol and pulsatile GnRH were required to increase GnRH receptor expression within 24 hours of treatment initiation. These results suggest an interaction between estradiol and GnRH is involved in increasing GnRH receptor expression during the periovulatory period. How progesterone, estradiol and, GnRH interact to increase GnRH receptors is unknown, but a possible candidate involved in mediating these interactions may be the cell specific transcription factor, steroidogenic factor-1 (SF-1). SF-1 mRNA increased within 24 hours of treatment of ewes with prostaglandin F₂(α) compared to ewes in the luteal phase of the estrous cycle. This suggests that progesterone may have an inhibitory effect on SF-1 mRNA. SF-1 mRNA was similar between ovariectomized ewes and ovariectomized ewes following hypothalamic-pituitary disconnection treated with estradiol and GnRH. Treatment with estradiol or GnRH alone did not increase SF-1 mRNA. The results of these experiments suggest that progesterone removal as well as the presence of estradiol and GnRH are required to increase GnRH receptor expression during the early follicular phase in the ewe. Further, the transcription factor, SF-1 may be involved in mediating the effects of these hormones on GnRH receptor expression.
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Von, Boetticher S. "Investigating the mechanism of transcriptional regulation of the gonadotropin-releasing hormone receptor (GnRHR) gene by dexamethasone." Thesis, Link to the online version, 2008. http://hdl.handle.net/10019/1796.
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Wormald, Patricia J. "GnRH and neuropeptide regulation of gonadotropin secretion from cultured human pituitary cells." Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27168.
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Gonadotropin-releasing hormone (GnRH) and its superactive analogues are currently being used in the treatment of a number of endocrine disorders, such as endometriosis, precocious puberty, infertility and prostatic cancer. Selection of these analogues for clinical use have been previously based on their activities in animal models. This thesis has therefore investigated the binding characteristics of the human GnRH receptor, in comparison to those of the rat receptor, as well as the activities of a number of GnRH analogues for stimulating luteinising hormone (LH) and follicle stimulating hormone (FSH) secretion from cultured human pituitary cells. The establishment of a human pituitary bioassay system has further made possible the investigation of the direct regulatory roles of GnRH and other neuropeptides in man. To date, such studies in man have been performed in vivo and are thus complicated by the simultaneous interactions of numerous modulators.
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Powell, R. C. "Evolution of the structure and function of vertebrate brain gonadotropin-releasing hormone." Master's thesis, University of Cape Town, 1986. http://hdl.handle.net/11427/27201.
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In this study, the structure and function of gonadotropin-releasing hormone (GnRH) in different vertebrate species, in the classes Aves, Reptilia and Pisces was investigated. Acetic acid extracts were subjected to gel filtration chromatography and semipreparative high performance liquid chromatography (HPLC) to partially purify the GnRHs. The GnRH immunoreactivity was then characterized by analytical HPLC, and by assaying HPLC fractions by radioimmunoassay with region-specific antisera generated against mammalian GnRH, Gln⁸-GnRH and Trp⁷,Leu⁸-GnRH and assessing luteinizing hormone (LH)-releasing activity of fractions in a chicken dispersed anterior pituitary cell bioassay. Five GnRH molecular forms have thusfar been structurally characterized in vertebrate brain. In mammals a GnRH with the structure pGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH₂ has been demonstrated in the hypothalamus (Matsuo et al., 1971; Burgus et al., 1972). Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were present in chicken hypothalamus (King and Millar, 1982a, 1982c; Miyamoto et al., 1983, 1984), Trp⁷,Leu⁸-GnRH in salmon brain (Sherwood et al., 1983) and Tyr³,Leu⁵,Glu⁶,Trp⁷,Lys⁸-GnRH in lamprey brain (Sherwood et al., 1986). In ostrich (Struthio camelus) hypothalamus two GnRHs with identical properties to Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH have been demonstrated, as well as four other LR-releasing factors with different chromatographic and immunological properties to any of the known naturally-occurring GnRHs. Since Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were also present in chicken hypothalamus it appears likely that these two GnRHs occur in all birds. In alligator (Alligator mississippiensis) brain only two GnRHs were detected. These forms co-eluted with Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH in two HPLC systems. They cross-reacted similarly to the two synthetic peptides with antisera directed against mammalian GnRH and Gln⁸-GnRH and released LH from chicken dispersed anterior pituitary cells in a similar manner to the synthetic peptides. The Archosaurs (alligators and crocodiles) are believed to be closely related to birds and therefore it seems likely that they should have identical GnRHs. In skink (Calcides ocellatus tiligugu) brain one GnRH, which co-eluted with His⁵,Trp⁷,Tyr⁸-GnRH, was demonstrated. Two other lizards (Cordylis nigra and Pordarcis s. sicula) have been studied (Powell et al., 1985; R.C. Powell, G. Ciarcia, V. Lance, R.P. Millar and J.A. King, submitted). In c. nigra four immunoreactive GnRHs were detected, two of which co-eluted released chicken LH similarly to, Trp⁷,Leu⁸-GnRH and with, and His⁵,Trp⁷,Tyr⁸-GnRH. In P. s. sicula a GnRH molecular form similar to Trp⁷,Leu⁸-GnRH occurred as well as two novel GnRHs. It thus appears that Gln⁸-GnRH does not occur in lower reptiles, but His⁵,Trp⁷,Tyr⁸-GnRH and/or Trp⁷,Leu⁸-GnRH do. His⁵,Trp⁷,Tyr⁸-GnRH appears to he a widespread GnRH, occurring in vertebrates as diverse as birds and elasmobranch fish. In dogfish (Poroderma africanum) brain seven factors, which stimulated release of LH from chicken dispersed anterior pituitary cells, were separated on analytical HPLC. Two of these factors were partially characterized as Trp⁷,Leu⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH. Three of the other forms cross-reacted with GnRH antisera, but appear to be novel GnRHs. In teleost (Coris julis) brain two GnRHs similar to Trp⁷,Leu⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were present. These two GnRHs therefore appear to occur in both fish species studied. Trp⁷,Leu⁸-GnRH is widespread amongst teleost fish (Jackson and Pan, 1983; Sherwood et al., 1983; Breton et al., 1984; Sherwood et al., 1984; King and Millar, 1985). From these data it seems evident that the mammalian GnRH molecular form occurs only in mammals and amphibians, Gln⁸-GnRH in birds and higher reptiles, and Trp⁷,Leu⁸-GnRH in gnathostomes. His⁵,Trp⁷, Tyr⁸-GnRH appears to he present in numerous different vertebrates. Tyr³,Leu⁵,Glu⁶,Trp⁷,Lys⁸-GnRH has thus far only been detected in lamprey brain. A number of novel GnRHs, whose structures have not been elucidated are present.
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Ely, Heather Ashlie. "A mechanism for gonadotropin-releasing hormone induction of c-Fos gene expression in pituitary gonadotrope cells." Diss., [La Jolla, Calif.] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1462104.
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Thesis (M.S.)--University of California, San Diego, 2009.Title from first page of PDF file (viewed March 19, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 66-72).
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李繼仁 and Kai-yan Lee. "Regulation of gonadotropin-releasing hormone and gonadotropin in goldfish, carassius auratus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31214332.
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Lee, Kai-yan. "Regulation of gonadotropin-releasing hormone and gonadotropin in goldfish, carassius auratus /." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18038165.
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Styger, Gustav. "The role of steroidogenic factor-1 (SF-1) in transcriptional regulation of the gonadotropin-releasing hormone (GnRH) receptor gene." Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52572.
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Thesis (MSc)--Stellenbosch University, 2001.ENGLISH ABSTRACT: The GnRH receptor is a G-protein-coupled receptor in pituitary gonadotrope cells. Binding of its ligand, GnRH, results in synthesis and release of gonadotropin hormones luteinizing hormone (LH) and follicle stimulating hormone (FSH). Steroidogenic factor 1 (SF-1), a transcription factor, binds to specific sites in the promoter region of gonadotropin genes, and thus regulates transcription of these genes. The promoter region of the GnRHreceptor gene contains two SF-1-like binding sites, one at -14 to -8 (site 1) and another at -247 to -239 (site 2), relative to the methionine start codon. The role played by these two SF-1-like sites in basal transcription of the mouse GnRH receptor (mGnRH-R) gene in a pituitary precursor gonadotrope cell line, aT3 cells, was the first area of investigation during this study. Luciferase reporter constructs containing 580 bp of mGnRH-R gene promoter were prepared, where SF-1-like sites were either wildtype or mutated. Four such constructs were made, i.e. wildtype (LG), site 1 mutant (LGM1), site 2 mutant (LGM2) and mutated site 1 plus site 2 (LGM1/2). These constructs were transfected into aT3 cells to determine the effect of mutations of sites 1 and/or 2 on the basal expression of the mGnRH-R gene. Mutation of either site 1 or site 2 had no effect on basal expression of the mGnRH-R gene. It was found that only upon simultaneous mutation of both sites 1 and 2, a 50% reduction in basal transcription took place. The implications of this is that SF-1 protein seems to only require one intact DNA-binding site, to mediate basal transcription of the mGnRH-R gene, suggesting that these two sites lie in close proximity during basal transcription. The effect of the protein kinase A (PKA) pathway on the endogenous mGnRH-R gene was also investigated by incubating non- , transfected aT3 cells with the PKA activators, forskolin and 8-Br-cAMP. Similar incubations were also performed on the wild type and mutated site 1 constructs transfected into pituitary gonadotrope aT3 cells. It was found that forskolin and 8-Br-cAMP were able to increase endogenous mGnRH-R mRNA levels in a concentration-dependent fashion, showing that endogenous GnRH receptor gene expression is stimulated via a protein kinase A pathway. Similar results were obtained with the wildtype promoter construct, showing that the protein kinase A pathway stimulates transcription of the promoter. This effect was only seen with wild type and not with the mutated site 1. These results are consistent with a role for a SF-1-like transcription factor in mediating the protein kinase A effect via binding to the site 1 at position -14 in the GnRH receptor gene. A separate investigation was performed to determine whether 25-hydroxycholesterol (25-0HC) is a ligand for SF-1, by incubating aT3 cells transfected with the various constructs with 25-0HC. Results show a dose-dependant response, with an increase in gene expression at 1 μM and a decrease at higher concentrations, for both mutant and wild type constructs. This suggests that, if SF-1 is indeed the protein binding to sites 1 and 2, then 25-0HC is not a ligand for SF-1 protein in aT3 cells and that the effect of 25-0HC on the mGnRH-R gene is not mediated via site 1. The results indicate that these decreases of expression at the higher concentrations may be due to cytotoxic effects. Towards the end of the study the laboratory obtained a luminoskan instrument with automatic dispensing features. Optimisation studies on the luciferase and β-Gal assays were performed on the luminoskan in a bid to decrease experimental error. It was found that automation of these assays resulted in a decrease in experimental error, showing that future researchers could benefit substantially from these optimisation studies.
AFRIKAANSE OPSOMMING: Die GnRH reseptor is 'n G proteïen-gekoppelde reseptor in pituitêre gonadotroopselle. Binding van die ligand, GnRH, lei tot die sintese en vrystelling van die gonadotropien hormone, luteïniserende hormoon (LH) en follikel stimulerende hormoon (FSH). Steroidogeniese faktor-t (SF-1) is 'n transkripsie faktor wat aan spesifieke areas in die promotergebied van die gonadotropien hormone bind, en dus transkripsie van hierdie gene reguleer. Die promotergebied van die GnRH reseptor geen bevat twee SF-1 bindings areas, een by -14 to -8 (area 1) asook by -247 to -239 (area 2), relatief to die metionien beginkodon. Die rol wat hierdie twee SF-1 areas speel in basale transkripsie van die muis GnRH reseptor (mGnRH-R) geen in 'n pituïtêre voorloper gonadotroop sellyn, aT3 selle, was die eerste gebied van ondersoek gedurende hierdie studie. Plasmiede bestaande uit die 580 basispaar mGnRH-R promoter verbind aan 'n lusiferase geen is vervaardig, waar SF-1-soortige areas enersyds onveranderd gelaat is, of gemuteer is. Vier sulke plasmiede is vervaardig, nl. onveranderd (LG), area 1 mutant (LGM1), area 2 mutant (LGM2) en gemuteerde area 1 plus area 2 (LGM1/2). Hierdie plasmiede is gebruik om aT3 selle te transfekteer om die effek van mutasies van areas 1 en/of 2 op die basale ekspressie van die mGnRH-R geen te ondersoek. Daar is gevind dat mutasies van areas 1 of 2 geen effek op basale ekspressie op die bogenoemde geen gehad het nie. Slegs tydens gelyktydige mutasie van areas 1 en 2 het 'n 50% vermindering in basale transkripsie plaasgevind. Die implikasies hiervan is dat die SF-1 proteïen blykbaar slegs een volledige DNA-bindingsarea benodig om basale transkripsie van die mGnRH-R geen te reguleer. Dit wil dus voorkom of hierdie twee areas baie na aan mekaar geposisioneer is tydens basale transkripsie. Die effek van die proteïen kinase A (PKA) roete op die natuurlike mGnRH-R geen is ook ondersoek tydens inkubasie van nie-getransfekteerde aT3 selle met die PKA akiveerders, forskolin en 8-Br-cAMP. Soortgelyke inkubasie is ook gedoen op die onveranderde en gemuteerde area 1 plasmiede wat in aT3 selle getransfekteer is. Daar is gevind dat forskolin en 8-Br-cAMP daarin geslaag het om die natuurlike mGnRH-R geen mRNA vlakke op 'n konsentrasie-afhanklike wyse te vermeerder. Hierdie resultaat dui daarop aan dat die natuurlike mGnRH-R geen se ekspressie gestimuleer kan word via 'n proteïen kinase A roete. Soortgelyke resultate is verkry met die onveranderde promoter plasmied en dit wys ook daarop dat proteïen kinase A transkripsie deur die promoter kan stimuleer. Hierdie effek was slegs aanwesig met die onveranderde en nie met die gemuteerde area 1 plasmied nie. Die resultate stem ooreen met 'n rol vir SF-1 transkripsie faktor in die regulering van proteren kinase A effek deur middel van binding aan die area 1 by posisie -14 in die GnRH-R geen. 'n Afsonderlike ondersoek is gedoen om vas te stel of 25-hidroksiecholesterol (25-0HC) 'n ligand vir SF-1 is deur getransfekteerde aT3 selle met 25-0HC te inkubeer. Resultate toon 'n dosis-afhanklike respons met 'n verhoging in geen ekspressie by 1 μM en 'n verlaging met hoër konsentrasies vir beide onveranderde en gemuteerde plasmiede. Dit impliseer dat, indien SF-1 wel die faktor is wat aan areas 1 en 2 bind, 25-0HC nie die ligand vir SF-1 proteren in aT3 selle is nie en dat die effek van 25-0HC op die mGnRH-R geen nie gereguleer word via area 1 nie. Die verlaging in ekspressie gevind by die hoër konsentrasies is dalk die gevolg van sitotoksiese effekte. Teen die einde van die studie het die laboratorium luminoskan toerusting met outomatiese pipettering verkry. Optimiseringstudies van die lusifirase en β-Galtoetse is met die luminoskan gedoen in 'n poging om eksperimentele foute te minimaliseer. Daar is gevind dat outomatisering van hierdie toetse wel gelei het tot 'n verlaging in eksperimentele foute. Toekomstige navorsers kan dus grootliks voordeel trek uit hierdie optimiseringstudies.
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Nicola, Angela Cristina de [UNESP]. "Atividade dos neurônios noradrenérgicos do Locus coeruleus e o conteúdo de GnRH em ratas Wistar acíclicas." Universidade Estadual Paulista (UNESP), 2013. http://hdl.handle.net/11449/92094.
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000742177.pdf: 1654502 bytes, checksum: 866898964213e96038c110158bf8a746 (MD5)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação para o Desenvolvimento da UNESP (FUNDUNESP)
As alterações nos componentes reprodutivos do eixo hipotálamo-hipófise-gônadas em muitas fêmeas de mamíferos determinam a transição gradual de ciclos reprodutivos regulares para ciclos irregulares, com perda de fertilidade. A interação dos neurônios do hormônio liberador de gonadotrofinas (GnRH) e esteróides gonadais representa função chave na neurobiologia do envelhecimento, pois a sobreposição temporal da senescência endócrina e neural está mecanicamente interligada pelas alças de retroalimentação. Estímulos do locus coeruleus (LC) para a área pré-óptica (APO) e eminência mediana são essenciais para a liberação das gonadotrofinas e seus neurônios apresentam receptores para estrógeno e progesterona, sugerindo controle dos esteróides ovarianos. Neste estudo foi avaliado a atividade de células neuronais localizadas em áreas e núcleos envolvidos com o controle de ação dos neurônios GnRH de ratas Wistar no período de transição para a aciclicidade. Para este trabalho foram utilizadas fêmeas Wistar cíclicas (4 meses) e acíclicas (18-20 meses) submetidas à decapitação ou perfusão às 10, 14 e 18 h na fase do diestro. Após serem retirados, os cérebros dos animais decapitados foram congelados e armazenados para posterior determinação do conteúdo de GnRH hipotalâmico e do conteúdo de noradrenalina e dopamina na APO. Os cérebros perfundidos foram cortados seriadamente em secções coronais de 30 μm para a APO e o LC e...
Changes in reproductive components of the hypothalamic-pituitary-gonadal axis in many female mammals determine the gradual transition from regular reproductive cycles to irregular cycles, with loss of fertility. The interaction of neurons of gonadotropin-releasing hormone (GnRH) and gonadal steroids represents key role in the neurobiology of aging, because the temporal overlap of endocrine and neural senescence is mechanically interconnected by feedback loops. Stimulation of the locus coeruleus (LC) for the preoptic area (POA) and median eminence are essential for the release of gonadotropins and their neurons have receptors for estrogen and progesterone, suggesting control of ovarian steroids. Therefore, in this study we evaluated the activity of neuronal cells located in areas and nuclei involved in the control of action of GnRH neurons of female rats during the transition to acyclicity. For this study, we used cyclic female (4 months) and acyclic (18-20 months) rats underwent perfusion or decapitation at 10, 14 and 18 h of diestrus day. The brains from decapitated animals, after removed, were frozen and stored for subsequent determination of the hypothalamic GnRH content and the noradrenaline and dopamine content in the POA. The perfused brains were serially cut into coronal sections of 30 μm to POA and LC and subsequently submitted to immunohistochemical labeling for Fos (FRA) and FRA / TH, respectively. For quantitative analysis of the POA were considered plates containing AVPe being the counting of neurons FRA-ir performed from the insertion of the box with...
FAPESP: 12/14464-6
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Nicola, Angela Cristina de. "Atividade dos neurônios noradrenérgicos do Locus coeruleus e o conteúdo de GnRH em ratas Wistar acíclicas /." Araçatuba, 2013. http://hdl.handle.net/11449/92094.
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Orientador: Rita Cássia Menegati DornellesCo-orientador: Janete Aparecida Anselmo-Franci
Banca: Maristela de Oliveira Poletini
Banca: Jacqueline Nelisis Zanoni
Resumo: As alterações nos componentes reprodutivos do eixo hipotálamo-hipófise-gônadas em muitas fêmeas de mamíferos determinam a transição gradual de ciclos reprodutivos regulares para ciclos irregulares, com perda de fertilidade. A interação dos neurônios do hormônio liberador de gonadotrofinas (GnRH) e esteróides gonadais representa função chave na neurobiologia do envelhecimento, pois a sobreposição temporal da senescência endócrina e neural está mecanicamente interligada pelas alças de retroalimentação. Estímulos do locus coeruleus (LC) para a área pré-óptica (APO) e eminência mediana são essenciais para a liberação das gonadotrofinas e seus neurônios apresentam receptores para estrógeno e progesterona, sugerindo controle dos esteróides ovarianos. Neste estudo foi avaliado a atividade de células neuronais localizadas em áreas e núcleos envolvidos com o controle de ação dos neurônios GnRH de ratas Wistar no período de transição para a aciclicidade. Para este trabalho foram utilizadas fêmeas Wistar cíclicas (4 meses) e acíclicas (18-20 meses) submetidas à decapitação ou perfusão às 10, 14 e 18 h na fase do diestro. Após serem retirados, os cérebros dos animais decapitados foram congelados e armazenados para posterior determinação do conteúdo de GnRH hipotalâmico e do conteúdo de noradrenalina e dopamina na APO. Os cérebros perfundidos foram cortados seriadamente em secções coronais de 30 μm para a APO e o LC e...
Abstract: Changes in reproductive components of the hypothalamic-pituitary-gonadal axis in many female mammals determine the gradual transition from regular reproductive cycles to irregular cycles, with loss of fertility. The interaction of neurons of gonadotropin-releasing hormone (GnRH) and gonadal steroids represents key role in the neurobiology of aging, because the temporal overlap of endocrine and neural senescence is mechanically interconnected by feedback loops. Stimulation of the locus coeruleus (LC) for the preoptic area (POA) and median eminence are essential for the release of gonadotropins and their neurons have receptors for estrogen and progesterone, suggesting control of ovarian steroids. Therefore, in this study we evaluated the activity of neuronal cells located in areas and nuclei involved in the control of action of GnRH neurons of female rats during the transition to acyclicity. For this study, we used cyclic female (4 months) and acyclic (18-20 months) rats underwent perfusion or decapitation at 10, 14 and 18 h of diestrus day. The brains from decapitated animals, after removed, were frozen and stored for subsequent determination of the hypothalamic GnRH content and the noradrenaline and dopamine content in the POA. The perfused brains were serially cut into coronal sections of 30 μm to POA and LC and subsequently submitted to immunohistochemical labeling for Fos (FRA) and FRA / TH, respectively. For quantitative analysis of the POA were considered plates containing AVPe being the counting of neurons FRA-ir performed from the insertion of the box with...
Mestre
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Flanagan, Colleen A. "Gonadotropin releasing hormone receptor ligand interactions." Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27029.
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The decapeptide, gonadotropin releasing hormone (GnRH), is the central regulator of reproductive function. It binds to receptors on the gonadotrope cells of the pituitary and stimulates release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). Eleven different structural forms of GnRH have now been identified in various animal species. Chimaeric analogues of some of the variant forms of GnRH were synthesized in order to study the functional significance of the most common amino acid substitutions, which occur in positions 5, 7 and 8. Peptide binding affinities for sheep and rat GnRH receptors and potencies in stimulating LH and FSH release from cultured sheep pituitary cells and LH release from cultured chicken pituitary cells were measured. Histidine in position 5 decreased LH releasing potency in chicken cells, but slightly increased receptor binding affinity in rat and sheep membranes. Tryptophan in position 7 had minimal effect on GnRH activity in mammals, but increased LH release in chicken cells. Although differences in the structural requirements of mammalian and chicken GnRH receptors were anticipated, it was also found that rat GnRH receptors exhibited higher affinity for analogues with Tryptophan in position 7, than did sheep GnRH receptors. Substitutions in position 8 revealed the most marked differences in the structural requirements of mammalian and chicken GnRH receptors. Arginine was required for high GnRH activity in mammalian systems, but analogues with neutral substitutions in position 8 were more potent in chicken pituitary cells. The tolerance of position 8 substitutions, combined with the relatively small effects, in chicken cells, of incorporating a D-amino acid in position 6, indicate that the chicken GnRH receptor is less stringent than mammalian receptors in its recognition of peptide conformation. To examine how changes in ligand structure cause changes in receptor binding affinity and receptor activation, it was necessary to know the structures of the GnRH receptors. A protocol was developed for the purification of GnRH binding proteins from detergent-solubilized pituitary membranes, by affinity chromatography. This procedure yielded a protein which migrated as a single band on sodium dodecyl sulfate polyacrylamide gel electrophoresis, but was different from the recently cloned GnRH receptor. To test the proposal that the arginine residue in mammalian GnRH interacts with an acidic receptor residue, eight conserved acidic residues of the cloned mouse GnRH receptor were mutated to asparagine or glutamine. Mutant receptors were transiently expressed in COS-1 cells and tested for decreased preference for Arg⁸-containing ligands by ligand binding and inositol phosphate production. One mutant receptor, in which the glutamate residue in position 301 was mutated, exhibited decreased affinity for mammalian GnRH. The mutant receptor also exhibited decreased affinity for [Lys⁸]-GnRH, but unchanged affinity for [Gln⁸]-GnRH compared with the wildtype receptor, and increased affinity for the acidic analogue, [Glu⁸]-GnRH. This loss of affinity was specific for the residue in position 8, because the mutant receptor retained hiszh affinity for analogues with favourable substitutions in positions 5, 6 and 7. Thus, the Glu³⁰¹ residue of the GnRH receptor plays a role in receptor recognition of Arg⁸ in the ligand, consistent with an electrostatic interaction between these two residues. The Glu³⁰¹ and Arg⁸ residues were not required for the high affinity interactions of conformationally constrained peptides. This indicates that an interaction which involves these two residues may induce changes in the conformation of GnRH after it has bound to the receptor.
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Gardner, Samantha. "Gonadotropin-releasing hormone targets Wnt signalling." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29112.
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This thesis describes a potential mechanism by which GnRH promotes the nuclear accumulation of β-catenin, activation of TCF-dependent transcription and up-regulation of Wnt target genes, c-Jun, Fra-1, Cyclin D1 and c-Mye. GnRH-induced nuclear accumulation of β-catenin and activation of β-catenin/TCF-dependent transcription was found to be dependent on a pathway utilising Gq-Phospholipase C (PLC)-Diacylglycerol (DAG)/Protein kinase C (PKC), and was found to be specifically dependent on the PKC δ isoform. GnRH was found to mediate the inactivation of Glycogen Synthase Kinase-3 (GSK-3), a protein serine/threonine kinase that regulates β-catenin degradation within the canonical Wnt signalling pathway. These results were observed in HEK293/GnRH receptor expressing cells and have been recapitulated in LβT2 and αT3-1 mouse gonadotrope cells, and then extended to various peripheral cell lines, sub-cultured prostate cells and whole prostate organ cultures. A potential mechanism of non-canonical Wnt/Ca2+ pathway activation by GnRH is described. GnRH was found to activate NFAT, a potential effecter of the non-canonical Wnt/Ca2+ pathway. GnRH-induced NFAT activation was found to be dependent on important mediators of the non-classical Wnt/Ca2+ pathway, including Gq, Ca2+, Calcineurin and PKC δ. Intriguingly, by expression of a dominant negative TCF construct, GnRH-induced NFAT activation was found to be TCF-dependent, thereby implicating TCF in targeting both Wnt/β-catenin and Wnt/Ca2+ signalling. This novel finding suggests that a TCF-NFAT interaction may exist that functions either, to inhibit β-catenin/TCF-dependent transcription through competition for nuclear TCF, or to synergistically regulate TCF- and NFAT-target gene expression.
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Van, Biljon Wilma. "The mammalian type II gonadotropin-releasing hormone receptor : cloning, distribution and role in gonadotropin gene expression." Thesis, Stellenbosch : University of Stellenbosch, 2006. http://hdl.handle.net/10019.1/17333.
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Dissertation (PhD)--University of Stellenbosch, 2006.ENGLISH ABSTRACT: Gonadotropin-releasing hormone (GnRH) is well known as the central regulator of the reproductive system through its stimulation of gonadotropin synthesis and release from the pituitary via binding to its specific receptor, known as the gonadotropin-releasing hormone receptor type I (GnRHR-I). The gonadotropins, luteinising hormone (LH) and follicle-stimulating hormone (FSH), bind to receptors in the gonads, leading to effects on steroidogenesis and gametogenesis. The recent finding of a second form of the GnRH receptor, known as the type II GnRHR or GnRHR-II, in non-mammalian vertebrates triggered the interest into the possible existence and function of a GnRHR-II in humans. The current study addressed this issue by investigating the presence of transcripts for a GnRHR-II in various human tissues and cells. While it was demonstrated that antisense transcripts for this receptor, containing sequence of only two of the three coding exons, are ubiquitously and abundantly expressed in all tissues examined, potentially full-length (containing all three exons), sense transcripts for a GnRHR-II were detected only in human ejaculate. Further analysis revealed that the subset of cells in the ejaculate expressing these transcripts is mature sperm. These findings, together with the reported role for GnRH in spermatogenesis and reproduction led to the further analysis of the presence of a local GnRH/GnRHR network in human and vervet monkey ejaculate or sperm. Indeed, such a network seems to be present in humans since transcripts for both forms of GnRH present in mammals, as well as transcripts for the GnRHR-I, are expressed in human ejaculate. Furthermore, transcripts for the GnRHR-II are expressed in both human and vervet monkey ejaculate. Thus, it would appear that locally produced GnRH-1 and/or GnRH-2 in the human male reproductive tract might mediate their effects on fertility via a local GnRHR-I, and possibly via GnRHR-II. Remarkably, in the pituitary, LH and FSH are present in the same gonadotropes, yet they are differentially regulated by GnRH under various physiological conditions. While it is well established that post-transcriptional regulatory mechanisms occur, the contribution of transcriptional regulation to the differential expression of the LHβ- and FSHβ-subunit genes is unclear. In this study, the role of GnRH-1 and GnRH-2 via the GnRHR-I and the GnRHR-II in transcriptional regulation of mammalian LHβ- and FSHβ genes was determined in the LβT2 mouse pituitary gonadotrope cell-line. It is demonstrated for the first time that GnRH-1 may affect gonadotropin subunit gene expression via GnRHR-II in addition to GnRHR-I, and that GnRH-2 also has the ability to regulate gonadotropin subunit gene expression via both receptors. Similar to other reports, it is shown that the transcriptional response to GnRH-1 of LHβ and FSHβ is low (about 1.4-fold for bLHβLuc and 1.2-fold for oFSHβLuc). In addition, evidence is supplied for the first time that GnRH-2 transcriptional regulation of the gonadotropin β subunits is also low (about 1.5-fold for bLHβLuc and 1.1-fold for oFSHβLuc). It is demonstrated that GnRH-1 is a more potent stimulator of bLHβ promoter activity as compared to GnRH-2 via the GnRHR-I, yet both hormones result in a similar maximum induction of bLHβ. However, GnRH-2 is a more efficacious stimulator of bLHβ transcription via the GnRHR-II than GnRH-1. No discriminatory effect of GnRH-1 vs. GnRH-2 was observed for oFSHβ promoter activity via GnRHR-I or GnRHR-II. By comparison of the ratio of expression of transfected oFSHβ- and bLHβ promoterreporters via GnRH-1 with that of GnRH-2, it is shown that GnRH-2 is a selective regulator of FSHβ gene transcription. This discriminatory effect of GnRH-2 is specific for GnRHR-I, as it is not observed for GnRHR-II, where GnRH-1 results in a greater oFSHβ- to-bLHβ ratio. These opposite selectivities for GnRHR-I and GnRHR-II on the ratios of oFSHβ:bLHβ promoter activity for GnRH-1 vs. GnRH-2 suggest a mechanism for fine control of gonadotropin regulation in the pituitary by variation of relative GnRHR-I vs. GnRHR-II levels. In addition, a concentration-dependent modulatory role for PACAP on GnRH-1- and GnRH-2-mediated regulation of bLHβ promoter activity, via both GnRHR-I and GnRHR-II, and of oFSHβ promoter activity, via GnRHR-I, is indicated. The concentration-dependent effects suggest the involvement of two different signalling pathways for the PACAP response. Together these findings suggest that transcription of the gonadotropin genes in vivo is under extensive hormonal control that can be finetuned in response to varying physiological conditions, which include changing levels of GnRH-1, GnRH-2, GnRHR-I and GnRHR-II as well as PACAP.
AFRIKAANSE OPSOMMING: Gonadotropien-vrystellingshormoon (GnRH) is bekend as die sentrale reguleerder van die voorplantingsisteem deur die stimulasie van gonadotropiensintese en - vrystelling vanaf die pituïtêre klier via binding aan ‘n spesifieke reseptor, die sogenaamde tipe I gonadotropien-vrystellingshormoonreseptor (GnRHR-I). Die gonadotropiene, lutineringshormoon (LH) en follikel-stimuleringshormoon (FSH), bind aan reseptore in die gonades waar dit steroïedogenese en gametogenese beïnvloed. Die onlangse ontdekking van ‘n tweede vorm van die GnRH-reseptor, bekend as die tipe II GnRHR of GnRHR-II, in nie-soogdier vertebrate het belangstelling in die moontlike bestaan en funksie van ‘n GnRHR-II in die mens gewek. Hierdie kwessie is aangeraak deur die teenwoordigheid van transkripte vir ‘n GnRHR-II in verskeie weefsel- en seltipes van die mens te ondersoek. Daar is aangetoon dat nie-sin transkripte vir hierdie reseptor, wat die DNA-opeenvolgings van slegs twee van die drie koderende eksons bevat het, oormatig uitgedruk word in al die weefseltipes wat ondersoek is. Daarteenoor is potensieel vollengte (bevattende al drie eksons) sin transkripte vir ‘n GnRHR-II in die mens slegs in semen gevind. Verdere analise het getoon dat dit volwasse sperma binne die semen is wat laasgenoemde transkripte uitdruk. Hierdie bevindinge, tesame met die aangetoonde rol vir GnRH in spermatogenese en reproduksie het gelei tot die verdere analise van die teenwoordigheid van ‘n lokale GnRH/GnRHR-netwerk in mens- en blouaapsemen of -sperm. So ‘n netwerk blyk om teenwoordig te wees in die mens, aangesien transkripte vir beide vorme van GnRH wat in soogdiere gevind word, asook transkripte vir die GnRHR-I, in menssemen uitgedruk word. Daarbenewens word transkripte vir die GnRHR-II uitgedruk in beide mens- en blouaapsemen. Dit wil dus voorkom asof lokaalgeproduseerde GnRH-1 en/of GnRH-2 in die manlike voortplantingstelsel van die mens hul effek op vrugbaarheid bemiddel via ‘n lokale GnRHR-I, en moontlik ook via GnRHR-II. Dit is opmerklik dat LH en FSH teenwoordig is in dieselfde gonadotroopselle van die pituïtêre klier en tog verskillend gereguleer word deur GnRH tydens verskeie fisiologiese kondisies. Terwyl dit bekend is dat post-transkripsionele reguleringsmeganismes teenwoordig is, is die bydrae van transkripsionele regulering tot die differensiële uitdrukking van die LHβ- en FSHβ-subeenheidgene minder duidelik. In hierdie studie is die rol van GnRH-1 en GnRH-2 via die GnRHR-I en die GnRHR-II in transkripsionele regulering van soogdier-LHβ- en -FSHβ-gene in die LβT2 muis pituïtêre gonadotroopsellyn bepaal. Dit is vir die eerste keer aangetoon dat GnRH-1 ‘n effek mag hê op gonadotropiensubeenheid-geenuitdrukking via GnRHR-II bykomend tot GnRHR-I, en dat GnRH-2 ook die vermoë besit om gonadotropiensubeenheid-geenuitdrukking via beide reseptore te reguleer. Soos deur ander studies aangetoon is die transkripsionele respons van LHβ en FSHβ tot GnRH-1 klein (ongeveer 1.4-voudig vir bLHβLuc en 1.2- voudig vir oFSHβLuc). Verder is daar vir die eerste keer bewys gelewer dat transkripsionele regulering van die gonadotropien β-subeenhede deur GnRH-2 ook gering is (ongeveer 1.5-voudig vir bLHβLuc en 1.1-voudig vir oFSHβLuc). Daar is aangetoon dat GnRH-1 ‘n sterker stimuleerder van bLHβ-promotoraktiwiteit is in vergelyking met GnRH-2 via die GnRHR-I, hoewel beide hormone tot ‘n soortgelyke maksimum induksie van bLHβ lei. GnRH-2 is egter ‘n meer effektiewe stimuleerder van bLHβ-transkripsie as GnRH-1 via die GnRHR-II. Geen verskille is gevind tussen die effekte van GnRH-1 en GnRH-2 op oFSHβ-promotoraktiwiteit via GnRHR-I of GnRHR-II nie. Wanneer die verhouding van uitdrukking van getransfekteerde oFSHβ- en bLHβ- promotor-verslaggewers via GnRH-1 met dié van GnRH-2 vergelyk is, is aangetoon dat GnRH-2 ‘n selektiewe reguleerder van FSHβ-geentranskripsie is. Hierdie diskriminasieeffek van GnRH-2 is spesifiek vir GnRHR-I aangesien dit nie vir GnRHR-II waargeneem word nie. GnRH-1 lei tot ‘n groter oFSHβ tot bLHβ-verhouding via GnRHR-II. Hierdie teenoorgestelde selektiwiteite van GnRHR-I en GnRHR-II op die verhoudings van oFSHβ tot bLHβ-promotoraktiwiteit vir GnRH-1 teenoor GnRH-2 suggereer dat daar ‘n meganisme bestaan vir die fyn regulering van gonadotropiene in die pituïtêre klier, deurdat die relatiewe vlakke van GnRHR-I teenoor GnRHR-II gevarieer word. Daarbenewens is ‘n konsentrasie-afhanklike moduleringsrol vir PACAP op GnRH-1- en GnRH-2-bemiddelde regulering van bLHβ-promotoraktiwiteit aangetoon, via beide GnRHR-I en GnRHR-II, asook op oFSHβ-promotoraktiwiteit via GnRHR-I. Hierdie konsentrasie-afhanklike effekte dui op die betrokkenheid van twee verskillende seinpadweë vir die PACAP-respons. Tesame suggereer hierdie bevindinge dat transkripsie van die gonadotropiengene in vivo onder ekstensiewe hormonale kontrole is wat verfyn kan word in respons to veranderlike fisiologiese kondisies. Laasgenoemde sluit veranderende vlakke van GnRH-1, GnRH-2, GnRHR-I en GnRHR-II asook PACAP in.
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顔秀慧 and S. W. Ngan. "Transcriptional regulation of the human gonadotropin releasing hormonereceptor gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31240847.
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Chen, Junling. "Ligand-independent activation of steroid hormone receptors by gonadotropin-releasing hormone." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/34980.
Full textAbstract:
Nuclear receptors including estrogen receptors (ERs) and progesterone receptors (PRs) are
activated by their ligands as well as by signaling pathways in response to peptide hormones and growth factors. In gonadotrophs, gonadotropin releasing hormones (GnRHs) act via the GnRH receptor (GnRHR). Both GnRH-I and GnRH-II activate an estrogen response element (ERE)-driven luciferase reporter gene in LβT2 mouse pituitary cells, and GnRH-I is more potent in this regard. The ERα is phosphorylated at Ser¹¹⁸ in the nucleus and at Ser¹⁶⁷ in both nucleus and cytoplasm after GnRI-I treatments, and this coincides with increased ERct binding to its co-activator, the P300/CBP-associated factor (PCAF). Most importantly, both GnRH subtypes robustly up-regulate expression of the immediate early response gene, Fosb, while co-treatment with ERα siRNA or PCAF siRNA attenuates this effect. This appears to occur at the transcriptional level because co-recruitment of ERα and PCAF to an ERE within the endogenous Fosb promoter is increased by GnRH treatments, as shown by chromatin
immunoprecipitation assays. Furthermore, cross-talk between GnRH-I and PR accentuates
gonadotropin production. GnRH-I activates a progesterone response element (PRE)-driven
luciferase reporter gene and gonadotropin a subunit (Gsua) gene expression in two mouse
gonadotroph cell lines, αT3-1 and LβT2. Up-regulation of the PRE-luciferase reporter gene
by GnRH-I is attenuated by pre-treatment with protein kinase A (H89) and protein kinase C
(GF109203X) inhibitors, while only GF109203X inhibits GnRH-1-induced Gsua mRNA levels. In both cell lines within the same time-frame, knockdown of PR levels by siRNA reduces GnRH-I activation of Gsua mRNA levels by approximately 40%. Both GnRH-I and GnRH-II also increase mouse Gnrhr-luciferase promoter activity and this is significantly
reduced by knockdown of PR in LβT2 cells. We conclude that the effects of GnRH-I on Fosb
and Gsua expression, as well as mouse Gnrhr promoter activity in mouse gonadotrophs are
mediated by ligand-independent activation of ERα and PR. These ligand-independent effects
of GnRHs on steroid hormone receptor function may influence the magnitude of changes in
the expression of specific genes in the pituitary during the mouse estrous cycle, which in this
context may serve as a model in the human menstrual cycle.
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Ngan, S. W. "Transcriptional regulation of the human gonadotropin releasing hormone receptor gene /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21687584.
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Wehmeyer, Lance. "Investigating crosstalk in lipid rafts between the glucocorticoid receptor and gonadotropin-releasing hormone receptor signaling pathways in a gonadotrope cell line." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/11346.
Full textAbstract:
Includes abstract.Includes bibliographical references (leaves 121-158).
A recent study from the Hapgood laboratory demonstrated the presence of a novel crosstalk mechanism between the glucocorticoid receptor (GR) and gonadotropin-releasing hormone receptor (GnRHR), indicating an additional direct mechanism for the effects of stress on reproduction. The present study investigated whether this crosstalk between the GR and GnRHR involves the co-localization of these receptors to lipid rafts, providing a specialized distinct region where the receptors can be in close proximity and reciprocally modulate each other’s signaling pathways.
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Armstrong, Stephen Paul. "Pulsatile Gonadotrophin-releasing Hormone Receptor Signalling." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526055.
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Vrisman, Dayane Priscila. "Indução da ovulação e funcionalidade do corpo lúteo em novilhas Nelore pré-púberes /." Jaboticabal, 2017. http://hdl.handle.net/11449/150726.
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Orientador: Maria Emilia Franco OliveiraCoorientador: Pedro Paulo Maia Teixeira
Coorientador: Fábio Morato Monteiro
Banca: Pietro Sampaio Baruselli
Banca: Lindsay Unno Gimenes
Resumo: Devido a comum ocorrência de regressão prematura (RP) do corpo lúteo (CL) em novilhas após primeira ovulação (OV), os objetivos do estudo foram: 1) acompanhar a dinâmica lútea após indução da OV em novilhas Nelore pré-púberes e 2) determinar diferenças relacionáveis a funcionalidade dessa estrutura. Cinquenta e sete fêmeas (289,61±32,28 kg, ECC de 5,66±0,65 e 17,47±0,81 meses de idade) foram divididas em dois grupos de tratamento para indução da OV. No grupo GP4+GnRH foi utilizado dispositivo intravaginal de progesterona (P4) de 3º uso por 10 dias e, 48 horas após remoção, aplicado 0,02mg de acetato de buserelina (GnRH), e no grupo GGnRH foi utilizado somente o GnRH. Os CLs formados foram acompanhados pela ultrassonografia a cada dois dias até a sua regressão funcional (diminuição do sinal vascular do Doppler colorido e concentrações de P4 abaixo de 1 ng/mL), sendo determinado para cada dia o diâmetro, área, valores numéricos (VPN) e heterogeneidade dos pixels e percentual (%) de vascularização. A velocidade do pico sistólico, velocidade diastólica final, índice de resistência e o índice de pulsatilidade (IP) da artéria ovariana também foram determinados para cada avaliação, além da concentração sérica de P4. Essas características foram comparadas entre os tratamentos, funções dos CLs (duração normal ou regredido prematuramente), dias das avaliações e suas interações, utilizando o procedimento MIXED do programa SAS (p≤0,05). Três animais de cada tratamento não responderam ao ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Due to the common occurrence of premature regression (PR) of the corpus luteum (CL) in heifers after the first ovulation (OV), the aims of this study were to: 1) monitor the luteal dynamics after OV induction in prepubertal Nellore heifers, and 2) determine differences related to the functionality of this structure. Fifty-seven females (BW 289.61±32.28 kg, BCS 5.66±0.65 and 17.47±0.81 months old) were divided into two treatment groups for OV induction. In the group GP4+GnRH, an intravaginal progesterone (P4) device of 3rd use was used for 10 days and, 48 hours after its removal 0.02 mg of buserelin acetate (GnRH) was applied, and in the GGnRH group only GnRH was used. Formed CLs were monitored via ultrasonography every two days until functional regression (decrease of the vascular signal of color Doppler and serum P4 concentrations below 1 ng/mL), being determined for each day the diameter, area, numerical values (NV) and heterogeneity of the pixels, and vascularization percentage (%). The systolic and diastolic peak velocity, resistance and pulsatility index (PI) of the ovarian artery were also determined for each day in addition to the serum P4 concentration. These characteristics were compared between treatments, CLs functions (normal duration or prematurely regressed), days of evaluations and their interactions, using the MIXED procedure of SAS program (p≤0.05). Three animals from each treatment did not respond to the OV inductor (6/57=11%), which determined an ovulation ... (Complete abstract click electronic access below)
Mestre
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Jeoung, Myoungkun. "IDENTIFICATION AND CHARACTERIZATION OF CONTACT SITES BETWEEN HUMAN CHORIONIC GONADOTROPIN AND LUTEINIZING HORMONE/CHORIOGONADOTROPIN RECEPTOR." Lexington, Ky. : [University of Kentucky Libraries], 2003. http://lib.uky.edu/ETD/ukybiol2003d00086/MJ.pdf.
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Thesis--University of Kentucky (Ph. D.), 2003.Title from document title page. Document formatted into pages; contains vii, 65 p. : ill. Includes abstract and vita. Includes bibliographical references (p. 60-65).
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Cronin, A. S. "Neurotrophic responses of developing Gonadotropin-releasing hormone neurons." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598166.
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The studies described in this thesis investigated the hypothesis that the development of GnRH neurite outgrowth is promoted by BDNF. The objectives were to establish whether BDNF and its receptor TrkB were expressed in regions associated with developing GnRH neurons, and then to ascertain whether BDNF elicited neurotrophic effects in GnRH neurons. In situ hybridisation revealed that during development from E12.5 to adult, BDNF mRNA was found throughout the hypothalamus, from the POA to the medial basal hypothalamus. TrkB mRNA (which encodes the receptor for BDNF) was found in the region of the olfactory tracts and bulbs at E14.5-16.5, and throughout the brain from E16.5 to adulthood. Furthermore, the majority of cultured embryonic GnRH cells were immunoreactive for TrkB. These primary cell cultures were used to investigate the actions of BDNF on GnRH neurite outgrowth. Treatment with BDNF for 39 hours induced a significant increase in the length of neurites, but had no discernible affect on branching. Subsequent investigations into the signalling pathway by which BDNF may exert this response revealed induction of phospho-Ca2+/cAMP response element-binding protein (pCREB) in GnRH and non-GnRH cells following an acute BDNF treatment. BDNF is known to induce phosphorylation of CREB in other neuronal types via the Ras-microtubule associated protein kinase/extracellular-regulated kinase (Ras-MAPK/ERK) pathway which also results in neurite outgrowth, so the response to BDNF of ERK, an upstream MAP kinase of CREB, was also tested in GnRH cells. It was discovered that pCREB was induced in GnRH cells following treatment with BDNF, but this was not associated with induction of pERK, though BDNF treatment did stimulate pERK in neighbouring non-GnRH cells. In summary, GnRH cells possess the receptor for BDNF, TrkB, and that during their development, the neurites they elaborate course through BDNF-rich areas of the brain.
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Von, Schalburg Kristian Robert. "The gonadotropin-releasing hormone gene : characterization, regulation and expression in two salmonids." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ36651.pdf.
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Neto, Acácio Pinto da Silveira. "Análise dos genes LIN28B, KISS1 e KISS1R em crianças com puberdade precoce central idiopática." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5166/tde-27102011-104731/.
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A puberdade é um processo biológico complexo do desenvolvimento sexual que tem início no final da infância e se caracteriza pela maturação do eixo hipotálamo-hipófise-gonadal, pelo desenvolvimento dos caracteres sexuais secundários, aceleração do crescimento e finalmente pela capacidade reprodutiva. Nos últimos anos, o peptídeo kisspeptina e seu receptor KISS1R têm sido fortemente envolvidos na regulação da secreção pulsátil do GnRH hipotalâmico e, portanto, com o início da puberdade humana. Mutações nos genes KISS1R e KISS1 foram identificadas em crianças brasileiras com puberdade precoce central (PPC). Estudos em famílias e em irmãs gêmeas estimaram que 50-70% da variação na idade de menarca pode ser hereditária, porém, até pouco tempo atrás, não se tinha conhecimento de variantes genéticas comuns que influenciassem no tempo de puberdade. Recentemente, quatro estudos independentes de associação ampla do genoma estabeleceram que marcadores genéticos próximos ou dentro do gene LIN28B estavam relacionados com a idade da menarca em mulheres normais. Além disso, mutações recessivas no gene lin28 levaram ao desenvolvimento precoce no C. elegans. Camundongos que superexpressam Lin28a apresentaram um retardo no desenvolvimento sexual. Com base nesses achados, investigamos a presença de variantes conhecidas ou novas nos genes KISS1, KISS1R e LIN28B em um grupo de crianças portadoras de PPC idiopática com o intuito de estabelecermos a prevalência dessas mutações na etiologia do desenvolvimento sexual prematuro em humanos. Cento e sete crianças com PPC (101 meninas e 6 meninos) foram selecionados, incluindo casos esporádicos e familiares. A população controle consistiu de 200 indivíduos adultos com história de desenvolvimento puberal normal em idade apropriada. A região promotora e os três exons do gene KISS1, os cinco exons do gene K1SS1R e os quatro exons do gene LIN28B foram amplificados e submetidos à sequenciamento automático. Uma variante em homozigose no gene KISS1, descrita anteriormente por pesquisadores do nosso laboratório, p.H90D, foi identificada em mais três crianças não relacionadas, portadoras de PPC idiopática. Essa variante está localizada no exon 3 do KISS1, levando a substituição de uma histidina por um ácido aspártico na posição 90 da kisspeptina-1 (p.H90D), correspondendo à região amino-terminal da kisspeptina-54 e estava ausente em 200 controles brasileiros. Estudos prévios in vitro com a variante p.H90D não revelaram alterações na capacidade de ligação ou ativação do KISS1R e na resistência a degradação. As mutações ativadoras p.R386P do KISS1R e p.P74S da kisspeptina, previamente descritas em puberdade precoce central, não foram identificadas no estudo atual. Uma nova e rara variante em heterozigose no gene LIN28B, p.H199R, foi identificada em uma menina brasileira com PPC idiopática. Essa variante está localizada no exon 4 do LIN28B, levando a substituição de uma histidina conservada por uma arginina na posição 199 da proteína (p.H199R) e estava ausente em 200 controles brasileiros. O pai da paciente, que apresentou desenvolvimento puberal normal, era portador da mesma variante em heterozigose. Estudos in vitro revelaram que a variante p.H199R não afeta a função de LIN28B na regulação da expressão do miRNA let-7. Outra variante alélica no gene LIN28B foi identificada numa menina com PPC. Essa variante estava localizada no íntron 2 do gene e uma análise computacional demonstrou que ela não altera o sítio de splicing no RNA maduro. Em conclusão, observamos que mutações nos genes KISS1 e KISS1R têm uma baixa prevalência em crianças com puberdade precoce central idiopática. Descrevemos uma nova e rara variante no gene LIN28B (p.H199R) numa menina com puberdade precoce central e os estudos funcionais do LIN28B selvagem ou contendo a variante p.H199R sugeriram que essa variante não está relacionada ao fenótipo de puberdade precocePuberty is a complex biological process of sexual development that begins in the late childhood and it is characterized by the maturation of the hipothalamic-pituitary-gonadal axis, secondary sexual characteristics development, growth acceleration and acquisition of the reproductive capacity. Over the last years, the kisspeptin peptide and its receptor KISS1R have been envolved in the regulation of the pulsatile hipothalamic GnRH secretion and consequently with the beginning of the puberty human. Researchers from our laboratory identified mutations in the KISS1R and KISS1 genes in Brazilian children with central precocious puberty (CPP). Studies performed in families and twins estimated that 50%-70% of the variation in the menarce age can be hereditary, however, until last years, we did not have knowledgment of the influence of commun genetic variants in the puberty time. Recently, four independent Genome-Wide Association Studies established that genetic markers near or inside of LIN28B gene were related with the menarce age in normal women. Furthermore, recessive mutations in the LIN28B gene caused a precocious develpment in C. elegans. Interestingly, mouse that overexpress Lin28a exhibited a sexual development delay. Accordingly with these datas investigated the presence of known or new variants in the KISS1, KISS1R and LIN28B genes in a larger cohort of children with CPP to establish the prevalence of these mutations in the etiology of premature sexual development in humans. 107 children with CPP (101 girls and 6 boys) were selected, including sporadic and familial cases. The control population consisted of 200 adults with normal pubertal development. The promoter region and the three exons of KISS1 gene, five exons of KISS1R and four exons of LIN28B were amplified and automatically sequenced. A homozygous variant previously described by researchers from our laboratory in the KISS1 gene, p.H90D, was identified in more 3 no related children with CPP idiophatic. This variant is located in exon 3 of KISS1, resulting in substitution of a histidine to an aspartic acid at position 90 of kisspeptin-1 (p.H90D), in the amino-terminal region of the protein-54 and was absent in 200 Brazilian controls. Previous studies in vitro with the p.H90D variant did not show alterations in the binding or activation capacity and in the resistance to degradation. The activating mutations p.R386P of the KISS1R and p.P74S of the kisspeptin, previously described in central precocious puberty, were not identified in the present study. A new and rare heterozygous variant in the LIN28B gene, p.H199R, was identified in a Brazilian girl with CPP idiophatic. This variant is located in exon 4 of the LIN28B, resulting in substitution of a histidine to an arginine at position 199 of protein (p.H199R) and was absent in 200 Brazilian controls. Her father, which had normal pubertal development, carried the same heterozygous variant. Studies in vitro revealed p.H199R did not affect the function of Lin28B in the regulation of let-7 miRNA expression. Another allelic variant in the LIN28B gene was identified in a girl with CPP. This variant was located in intron 2 of the gene and an in silico analysis showed that it does not change the splicing site in mature RNA. In conclusion, we observed that mutations in the KISS1 and KISS1R genes have a low prevalence in children with idiopathic central precocious puberty. We described a new and rare variant in LIN28B gene (p.H199R) in a girl with central precocious puberty and functional studies of the wild LIN28B or containing p.H199R variant suggested that p.H199R variant of the LIN28B is not related to the precocious puberty phenotype
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Darko, Bošnjak. "Dijagnoza reproduktivnog statusa nazimica na osnovu ovarijalnog i estrusnog reagovanja, posle tretmana gonadotropnim, luteolitičkim i progestagenim hormonskim preparatima." Phd thesis, Univerzitet u Novom Sadu, Poljoprivredni fakultet u Novom Sadu, 2014. http://dx.doi.org/10.2298/NS20140123BOSNJAK.
Full textAbstract:
Determinacija reproduktivnog statusa priplodnih nazimica je važan faktor u tehnologiji njihovog odgoja i reproduktivnog iskorištavanja. Zbog toga je, u intenzivnoj proizvodnji svinja, potrebna primena efikasnih metoda dijagnoze reproduktivnog statusa nazimica. Klasična metoda testiranja pojave estrusa, kontaktom nazimica sa polno zrelim nerastom nije dovoljno precizna. Pokazalo se, naime, da se, zbog nepreciznosti ove metode, oko 30 do 40% priplodnih nazimica izlučuje iz priploda, sa dijagnozom „prolongirani preinseminacioni anestrus“, iako su ove nazimice uspostavile cikličnu ovarijalnu aktivnost. Ovo ima za posledicu značajne zootehnološke i ekonomske gubitke. Metoda real-time ultrazvučne dijagnoze reproduktivnog statusa je precizna, ali je skupa i nepraktična za masovnu primenu. Zbog toga je cilj ovog rada bio da se ispita mogućnost dijagnoze reproduktivnog statusa nazimica, na onsovu ovarijalnog i estrusnog reagovanja posle tretmana gonadotropnim, luteolitičkim i progestagenim hormonskim preparatima. Dobijeni rezultati pokazuju da postoji vrlo specifično ovarijalno i estrusno reagovanje polno nezrelih i polno zrelih nazimica, zavisno od primenjenog hormonskog tretmana. Rezultati primene luteolitičkih tretmana (PGF2α), pokazuju da ovaj tretman nije dovoljno precizan za dijagnozu reproduktivnog statusa nazimica. Tretman gonadotropnim hormonima (eCG i hCG) daje samo delimično precizne rezultate dijagnoze reproduktivnog statusa. Naime, polno nezrele nazimice reaguju dobrom sinhronizacijom estrusa, unutar prosečno 4 dana posle injekcije eCG. Međutim, trajanje intervala od injekcije eCG do pojave estrusa značajno varira, između 4 i 25 dana, kod polno zrelih nazimica. Vrlo precizna diferencijalna dijagnoza reproduktivnog statusa nazimica se postiže tretmanom sa progestagenim preparatima (Altrenogest, Regumate®). Polno nezrele nazimice ne reaguju sinhronizovanom ovulacijom i pojavom estrusa, posle tretmana progestagenim preparatom. Polno zrele nazimice, međutim, reaguju vrlo viskim stepeno sinhronizovane ovulacije i pojave estrusa, posle progestagenog tretmana. Dobijeni rezultati predstavljaju doprinos boljem poznavanju ovarijalnog i estrusnog reagovanja nazimica, posle tretmana egzogenim gonadotropinima, luteoliticima i progestagenima. Osim toga, ovi rezultati pružaju mogućnost precizne dijagnoze reproduktivnog statusa nazimimica u proizvodnim uslovima. Na taj način je moguće formulisati efikasniju tehnologiju reproduktivne eksploatacije nazimica i, time, povećati efikasnost intenzivne proizvodnje svinja.Determination of the replacement gilts reproductive status is an important factor of gilts reproductive utilization efficiency. Therefore, the intensive pig production, require the application of effective methods of gilts diagnosis reproductive status. Classical method for estrus manifestation testing, by gilts contact with sexually mature boar is not precise enough. It has been proved that, due to the inaccuracy of this method, about 30 to 40% gilts are culled from the breeding, with a diagnosis of "prolonged preinsemination anestrus," although these gilts was established cyclical ovarian activity. This results in significant zootechnical and economical losses. Method of real-time ultrasound diagnosis of reproductive status was accurate, but it is expensive and impractical in productive conditions. Therefore, the aim of this study was to investigate the possibility of gilts reproductive status diagnose, based on ovarian and estrous response after treatment with gonadotropin, luteolytic and progestogen hormonal preparations. Obtained results show that there is a very specific ovarian and estrous response of sexually immature and sexually mature gilts, depending on the applied hormonal treatment. Results of the luteolytic (PGF2α) treatment application, show that this treatment is not specific enough for the gilts reproductive status diagnosis. Treatment with gonadotropins (hCG and ECG) gives only a partial accurate diagnosis of gilts reproductive status. The sexually immature gilts respond with high level of estrus synchronization, within average 4 days after eCG injection. However, the interval from eCG injection to estrus manifestation varied between 4 and 25 days, in sexually mature gilts. Very accurate differential diagnosis of gilts reproductive status was achieved by treatment with progestogen preparations. Sexually immature gilts was not respond by synchronized estrus and ovulation, after treatment with progestogen preparation. Buth, sexually mature gilts respond with highly synchronized ovulation and estrus, within average 5 days after progestagenog treatment. The obtained results contribute to a better understanding of gilts ovarian and estrous responses to exogenous gonadotropins, luteolytics and progestagens treatment. In addition, these results provide an accurate ability for gilts reproductive status diagnosis in farms production conditions. On this way it is possible to formulate a more efficient technology of gilts reproductive exploitation and,thus, increase the efficiency of intensive pig production.
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Maze, Timothy D. "Development of the induced gonadotropin surge mechanism in the prepubertal heifer." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2525.
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Thesis (Ph. D.)--West Virginia University, 2002.Title from document title page. Document formatted into pages; contains viii, 71 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 61-70).
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Gaudron, Sylvie-Marylène. "Environment endocrine pheromone relationships in the control of reproduction in the scale worm Harmothoë imbricata (Polychaeta: Polynoidae) (L.)." Thesis, University of Newcastle Upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289277.
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Bettles, Stephen Paul. "Advancement of ovulation in yellowtail flounder, Pleuronectes ferrugineus, using gonadotropic hormone-releasing hormone analogue (GnRHa)." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23118.pdf.
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Kang, Sung Keun. "Role of gonadotropin-releasing hormone in the ovarian cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0020/NQ56568.pdf.
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Nelson, Shelley B. "Neuron-specific regulation of the gonadotropin-releasing hormone gene /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9951423.
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Stavrou, Emmanouil. "Regulation of FOXO transcription factors by gonadotropin-releasing hormone." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5686.
Full textAbstract:
G protein-coupled receptors (GPCRs) are a large family of trans-membrane receptors that transmit signals from extracellular stimuli to target intracellular signal transduction pathways. The gonadotropin-releasing hormone receptor (GnRH-R) is a GPCR which binds the decapeptide GnRH. In the pituitary gonadotrope, GnRH stimulates gonadotropin (LH and FSH) biosynthesis and secretion to regulate reproduction. GnRH and the GnRH-Rs are also present in many extra-pituitary tissues, although their role at these sites remains largely undetermined. GnRH-Rs are known to recruit a diverse array of signalling pathway mediators in different cell-types. These include; Gq/11-PLCβ-IP3/DAG-Ca2+/PKC signalling, monomeric G-proteins and integrins to mediate cell adhesion and migration, the activation of the major members of the mitogen-activated protein kinase (MAPK) super-family (extracellular signal-regulated kinase (ERK), c-Jun N-terminal Kinase (JNK) and p38MAPK), and β-catenin and other mediators of the canonical Wnt signalling pathway. This thesis describes the regulation of Forkhead Box O (FOXO) transcription factors by GnRH. The mammalian FOXO transcription factors, FOXO1, FOXO3a and FOXO4, are emerging as an important family of proteins that modulate the expression of genes involved in cell-cycle regulation, induction of apoptosis, DNA damage repair and response to oxidative stress. In this thesis, emphasis is placed on delineating the novel role of FOXO transcription factors in mediating two important and widely-researched areas of GnRH biology. Firstly, the role of FOXO transcription factors in mediating cell-growth inhibition in response to GnRH treatment is assessed in a heterologous HEK293/GnRH-R expressing cell line. Secondly, the role of transcription factors in regulating luteinising hormone-β (LHβ)-subunit expression is investigated in the LβT2 gonadotrope cell line. Activation of the GnRH-R can inhibit cell proliferation and induce apoptosis in certain tumour-derived cell lines. Several studies have reported that these events can occur as a result of changes in the expression profiles of specific cell-cycle regulatory and apoptotic genes, many of which are FOXO-target genes, including GADD45, FasL, p21Cip1 and p27Kip1. In this thesis, a role for FOXOs in targeting the expression of several of these genes in response to GnRH is assessed, highlighting a specific role for FOXO3a in mediating GADD45 and FasL expression. The signalling mechanisms through which FOXO3a regulates GADD45 expression in response to GnRH is also described. Finally, a stable FOXO3a-knock-down cell line was generated in order to further examine FOXO3a involvement in GnRH-induced cell-growth inhibition. GnRH is an essential regulator of the reproductive process by stimulating the synthesis of LH and FSH in pituitary gonadotropes, thereby regulating gametogenesis and steroidogenesis. Diverse signalling pathways have been reported to regulate LHβ-subunit expression in response to GnRH, including the ERK/JNK/p38MAPK cascades and factors such as Egr1, SF1 and β-catenin. In the second part of this thesis, the role of FOXOs in regulating LHβ-subunit expression in response to GnRH is described. The data presented suggests that GnRH can regulate LHβ-subunit expression through both indirect and direct FOXO3a-mediated mechanisms. Firstly, FOXO3a was found to regulate Egr1 expression to indirectly target LHβ-promoter activity. Secondly, a role for β-catenin as a FOXO3a co-factor to directly regulate LHβ-subunit expression, together with Egr1 and SF1, is also proposed. FOXO3a expression and sub-cellular localisation was assessed and demonstrated in LβT2 cells and in adult human male pituitary sections. The research presented in this thesis adds to the diversity of signalling pathways and mediators that GnRH can target in different cellular backgrounds in order to mediate a variety of cellular processes. The antiproliferative and apoptotic effects of GnRH on tumour-derived cell lines are well-documented, and this research highlights a novel role for FOXO3a in mediating these events. The regulation of gonadotropin synthesis remains an important topic of research, and the novel implication of FOXO3a in mediating LHβ-subunit expression adds further complexity to gonadotrope physiology.
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Vasilyev, Vyacheslav V. "Regulation of gonadotropin [beta]-subunit gene expression by gonadotropin-releasing hormone in immortalized pituitary cell lines /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3022216.
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Fernandes, S. M. (Sandra Maria). "Transcriptional regulation of the gonadotropin-releasing hormone receptor (GnRHR) gene by glucocorticoids." Thesis, Stellenbosch : Stellenbosch University, 2007. http://hdl.handle.net/10019.1/19595.
Full textAbstract:
Thesis (MSc)--University of Stellenbosch, 2007.ENGLISH ABSTRACT: The gonadotropin-releasing hormone (GnRH) receptor is a G-protein-coupled receptor in the pituitary gonadotropes and is an important control point for reproduction. GnRH binds to the GnRH receptor (GnRHR) resulting in the synthesis and release of follicle stimulating hormone (FSH) and luteinizing hormone (LH). The sensitivity of the pituitary to GnRH can be directly correlated with GnRHR levels. The mouse GnRHR promoter contains three cis elements containing binding sites for steroidogenic factor-1 (SF-1), namely site 1 (-15/-7), site 2 (-244/- 236) and site 3 (-304/-296) as well as an activator protein-1 (AP-1)-like consensus sequence (TGAGTCA) at position –336/-330. While sites 1 and 2 and the AP-1 site have been previously shown to be involved in regulation of transcription of the mouse GnRHR (mGnRHR) promoter in some cell lines, the role of site 3 has not been previously investigated. This study investigated whether transcription of the mGnRHR gene is regulated by GnRH and glucocorticoids in the LβT2 gonadotrope pituitary cell line, and the role therein of site 3 and the AP-1 site and their cognate proteins, using a combination of in vitro protein- DNA binding studies and promoter-reporter assays. The role played by site 3 and the AP-1 site in basal transcription of the mGnRHR gene in LβT2 cells was the first area of investigation during this study. Luciferase reporter plasmids containing 600 bp of the mGnRHR promoter were used where the site 3 and AP-1 sites were either wild-type or mutated. Two constructs were prepared from the wild-type construct, i.e. wild type (LG), site 3 mutant (m3) and AP-1 mutant (mAP-1). Transfection of LG, m3 and mAP-1 plasmids into LβT2 cells was carried out to determine the effect of these mutations on the basal expression of the mGnRHR gene. Mutation of site 3 resulted in a 1.5 fold increase in the transcriptional activity of the mGnRHR promoter. This suggests that site 3 plays a role in the inhibition of basal transcriptional levels of the mGnRHR promoter in LβT2 cells. Mutation of the AP-1 site resulted in a 50% decrease in basal transcriptional levels of the mGnRHR promoter in LβT2 cells. This suggests that the AP-1 site is involved in positively mediating the basal transcriptional response of the GnRHR promoter in LβT2 cells. Experiments towards the understanding of the mechanism of the cis elements (site 3 and AP-1 site) on the mGnRHR promoter were carried out along with the role of protein kinase A (PKA) pathways, proteins involved and the effect of varying doses for varying times of GnRH, as well as the overexpression of PKA and the SF-1 protein. It was found that site 3 and the AP-1 site are not involved in the GnRH response. Results suggest that site 3 is partially involved in the PKA response in LβT2 cells. Site 3 can bind SF-1 protein as shown via competitive electrophoretic mobility shift assays (EMSA). When EMSA’s were performed on the AP-1 site the findings were that the c-Fos protein was not involved in the activation of the AP-1 site. A factor was found to bind to the AP-1 site, which did not require the intact AP-1 site, suggesting that it could be the c-Jun protein that binds to the AP-1 site under basal conditions. Another area that was investigated was whether the mGnRHR promoter can be regulated by dexamethasone (dex) either via the AP-1 site or site 3. A dose and time-dependent increase in promoter activity was observed with dex. This effect appears to require site 3 and the AP-1 site, as shown by the complete loss of response when these sites were individually mutated, consistent with a functional interaction between site 3 and the AP-1 site in LβT2 cells.
AFRIKAANSE OPSOMMING: Die gonadotropienvrystellings hormoon (GnRH) reseptor is ‘n G-proteïen-gekoppelde reseptor in die pituitêre gonadotrope en is ’n belangrike beheerpunt vir reproduksie. GnRH bind aan die GnRH reseptor (GnRHR) met die gevolg dat follikel stimulerende hormoon (FSH) en luteïeniserende (LH) gesintetiseer en vrygestel word. Die sensitiwiteit van die pituitêre klier vir GnRH kan direk met GnRHR vlakke gekorreleer word. Die muis GnRHR promotor bevat drie cis elemente met bindingssetels vir steroïedogeniese faktor 1 (SF1), naamlik setel 1 (-15/-7), setel 2 (-244/-236) en setel 3 (-304/-296) sowel as ’n aktiveerder proteïen 1 (AP-1) tipe konsensus sekwens (TGAGTCA) in posisie -336/-330. Terwyl setels 1 en 2 en die AP-1 setel voorheen getoon is om by die regulering van transkripsie van die muis GnRHR (mGnRHR) promotor in party sellyne betrokke te wees, is die rol van setel 3 nog nie vantevore bestudeer nie. In hierdie studie is ondersoek of die transkripsie van die mGnRHR geen deur GnRH en glukokortikoïede in die LβT2 gonadotroop pituitêre sellyn gereguleer word, en die rol van setel 3 en die AP-1 setel en hulle binders, deur gebruik te maak van in vitro proteïen-DNA bindings studies en promotor-verslaggewer essais. Die rol wat setel 3 en die AP-1 setel in basale transkripsie van die mGnRHR gene in LβT2 selle gespeel het, was die eerste onderwerp wat in hierdie studie bestudeer is. Lusiferase verslaggewer plasmiede wat die eerste 600 bp van die mGnRHR promotor bevat het en waarin setel 3 en die AP-1 setels óf wilde tipe óf gemuteer was, is gebruik. Two konstrukte is vanaf die wilde tipe konstruk berei, naamlik wilde tipe (LG), ’n setel 3 mutant (m3) en ’n AP-1 mutant (mAP-1). Transfeksie van LG, m3 en mAP-1 plasmiede in LβT2 selle is deurgevoer om te bepaal wat die effek van hierdie mutasies op die basale ekspressie van die mGnRHR gene was. Mutasie van setel 3 het ’n 1.5-voudige toename in die transkripsionele aktiwiteit van die mGnRHR promotor tot gevolg gehad. Dit suggereer dat setel 3 ’n rol in die inhibisie van die basale transkripsievlakke van die mGnRHR promotor in LβT2 selle speel. Mutasie van die AP-1 setel het tot ‘n 50% verlaging in basale transkripsievlakke van die mGnRHR promotor in LβT2 selle gelei. Dit suggereer dat die AP-1 setel betrokke is in die positiewe bemiddeling van die basale transkriptionele respons van die GnRHR promotor in LβT2 selle. Eksperimente wat gemik was om die meganisme van die cis-elemente (setel 3 en die AP-1 setel) op die mGnRHR promotor te verklaar, asook om die rol van proteïen kinase A (PKA) paaie, proteïene daarby betrokke en die effek van varieende dosisse vir verskillende tye van GnRH, sowel as die oorekspressie van PKA en die SF-1 proteïen, is deurgevoer. Dit is gevind dat setel 3 en die AP-1 setel nie betrokke by die GnRH respons is nie. Die resultate suggereer dat setel 3 gedeeltelik betrokke is by die PKA respons van LβT2 selle. Setel 3 kan SF-1 proteïen bind soos getoon deur kompeterence elektroforetiese mobiliteits verskuiwings essais (EMSA). As EMSA’s deurgevoer is op die AP-1 setel is bevind dat die c-Fos proteïen nie betrokke is in die aktivering van die AP-1 setel nie. ’n Faktor is gevind om aan die AP-1 setel te bind wat nie ’n intakte AP-1 setel vereis het nie, wat gesuggereer het dat dit die c-Jun proteïen kan wees wat aan die AP-1 setel onder basale omstandighede bind. ’n Ander area wat ondersoek is, is of die GnRHR promotor gereguleer kan word deur deksametasoon (dex) óf via die AP-1 setel óf via setel 3. ’n Dosis en tyds-afhanklike toename in promotor aktiwiteit is waargeneem met dex. ’n Vereiste vir hierdie effek blyk om die teenwoordigheid van setel 3 en die AP-1 setel te wees, soos aangetoon deur die totale verlies aan response as hierdie twee setels individueel gemuteer is, en wat weereens in ooreenstemming met die funksionele interaksie tussen setel 3 en die AP-1 setel in LβT2 selle is.
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Cheung, Wai-ting. "Role of gonadotropin-releasing hormone of metastatic potential of ovarian cancer cells." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41634184.
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Hedberg, Alm Ylva. "Oestrus in the mare : with emphasis on deviant behaviour and adrenal gland function /." Uppsala : Department of Clinical Sciences, Swedish University of Agricultural Sciences, 2006. http://epsilon.slu.se/2006101.pdf.
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Dunn, Ian Chisholm. "The molecular biology of chicken gonadotrophin releasing hormone." Thesis, Open University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358005.
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Birnie, Linda M. "Gonadotrophin releasing hormone agonist and bovine ovarian function." Thesis, University of Aberdeen, 1995. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU543402.
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Imprecise control of bovine oestrus and ovulation and the highly variable nature of the superovulatory response impedes use of reproductive technologies. The use of GnRH to control antral follicle development and, hence, the oestrous cycle was investigated using 40 maiden heifers. Two GnRH agonist sources (Fertagyl; Receptal) were tested at two frequencies (24; 48 hour) and luteinising hormone release profile; and pattern of antral follicle and luteal development were monitored. Post cessation of GnRH treatment gonadotrophin was given at either a fixed or variable time relative to oestrus and superovulatory response assessed. Basal LH values were unaffected by treatment. Treatment at 24, but not 48 hour intervals resulted in reduced LH response values. Fertagyl 24 hour treatment stimulated increased numbers of follicles to grow to 3-5 mm and 6-9 mm but inhibited growth to 10 mm, maturation and ovulation. Four waves of follicular development occurred in GnRH agonist, but not control, animals. Luteolysis and oestrus was delayed in a proportion of animals challenged with prostaglandin during GnRH agonist treatment. Exogenous gonadotrophin given at fixed time (day 10 1 where oestrus = day 0) post cessation of treatment, elicited a greater superovulatory response than when given at variable time. There was a positive relationship between number of ovulations and viable embryos; and a negative relationship between body weight and progesterone concentration and consequently superovulatory response. High superovulatory responses were observed when gonadotrophin treatment was initiated in the presence of an active corpus luteum and the absence of a dominant follicle. It was concluded that GnRH agonist given every 24 hours depleted LH reserves; allowed selection and dominance of antral follicles, but not maturation and ovulation; precluded prostaglandin induced luteolysis in some animals; and increased ovulations and embryos when gonadotrophin treatment was at a fixed time.
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Hoo, L. C., and 何麗莊. "Transcriptional regulation of the human gonadotropin-releasing hormone(GnRH) II and GnRH receptor genes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29297011.
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Ma, Chi-him Eddie. "Molecular studies of gonadotropin releasing hormone receptors and estrogen receptors in goldfish (Carassius auratus)." Click to view the E-thesis via HKUTO, 2000. http://sunzi.lib.hku.hk/hkuto/record/B4257531X.
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馬智謙 and Chi-him Eddie Ma. "Molecular studies of gonadotropin releasing hormone receptors and estrogen receptors in goldfish (Carassius auratus)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B4257531X.
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Binder, April Kay. "The role of ß-catenin in the gonadotrope transcriptional network interactions with SF1 and TCF /." Pullman, Wash. : Washington State University, 2009. http://www.dissertations.wsu.edu/Dissertations/Fall2009/a_binder_090309.pdf.
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An, Beum-Soo. "Cross-talk between gonadotropin-releasing hormones and progesterone receptor in neuroendocrine cells." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/30705.
Full textAbstract:
Hypothalamic gonadotropin-releasing hormone (GnRH) is a decapeptide that plays a
pivotal role in mammalian reproduction. It is hypothesized that progesterone (P4) may regulate
GnRH I, GnRH II (a second form of GnRH) and GnRH I receptor (GnRH I R) at the
transcriptional level. Alternatively, GnRHs may stimulate transactivation of the progesterone
receptor (PR), thereby, modulating gonadotropin subunit gene expression. Treatment of human
neuronal cells with P4 suppressed GnRH I R promoter activity. This P4-stimulated inhibition
was enhanced when PR A was over-expressed. With respect to the two GnRHs, P4 increased
GnRH I mRNA levels, but did not significantly affect GnRH II gene expression.
Regulation of gonadotropin production involves interplay between steroids and neuropeptides,
thus we have examined the effects of GnRHs on PR activation in pituitary cells.
Treatment with GnRHs increased a progesterone response element (PRE)-luciferase reporter gene
activity. PR was phosphorylated at Ser294 and translocated into nucleus after GnRH treatment in
the absence of P4. Interactions between the PR and several coactivators were examined, and
treatment with GnRHs specifically induced PR: Steroid Receptor Coactivator-3 (SRC-3)
interaction. In chromatin immunoprecipitation assays, recruitment of PR and SRC-3 to the PRE
reporter gene was also increased by GnRHs. The knockdown of GnRH I R and SRC-3 levels by
siRNA treatment reduced GnRH-induced PR transactivation. Gonadotropin subunit gene
expression was evaluated following treatment with GnRHs, and common α-subunit and FSHβ
transcription were upregulated by GnRHs. We used siRNA for PR to examine the involvement of
PR in GnRH I-induced FSHβ gene expression. The effect of GnRH I on FSHβ, but not α -subunit
gene expression was reduced when siRNA targeting PR was introduced.
In summary, these results indicate that P4 is a potent regulator of GnRH I R and GnRH I at the transcriptional level, and this distinct effect of P4 on the GnRH system may be derived from the
differential action of PR A or PR B . Conversely, GnRHs can activate PR-mediated transcription in
the absence of P4, and this ligand-independent mechanism of PR additionally regulates FSHβ
subunit gene expression.Medicine, Faculty of
Obstetrics and Gynaecology, Department of
Graduate
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Keinänen, Kari. "The lutropin receptor identification, purification and structural characterization /." Oulu, Finland : University of Oulu, 1988. http://catalog.hathitrust.org/api/volumes/oclc/18696660.html.
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Pepa, Patricia Ann. "Repression of gonadotropin-releasing hormone gene expression by androgen receptor." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/fullcit?p1477926.
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Thesis (M.S.)--University of California, San Diego, 2010.Title from first page of PDF file (viewed July 16, 2010). Available via ProQuest Digital Dissertations. Includes bibliographical references (leaves 59-62).
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Cheng, Kwai Wa. "Transcription regulation of human gonadotropin-releasing hormone receptor gene expression." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61070.pdf.
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