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Dissertations / Theses on the topic 'Gonadotropin-Releasing hormones'

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Published: 7 December 2024
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1

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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2

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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3

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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4

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.

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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.<br>Medicine, Faculty of<br>Obstetrics and Gynaecology, Department of<br>Graduate
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5

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.<br>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.<br>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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6

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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7

Dromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation." University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.

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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.
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8

Kaplan, Hilton. "The control of prolactin secretion and the role of gonadotrophin releasing hormone in the production of concordant secretory spikes of luteinizing hormone and prolactin in the luteal phase of the menstrual cycle." Master's thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27203.

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The control of prolactin secretion is a complex interaction of peptides and neurotransmitters acting either in an inhibitory or stimulating way to effect final secretion of this hormone from the lactotrope cell in the anterior hypothalamus. These factors may act either directly on the lactotrope cell or indirectly by changing either dopamine restraint of prolactin secretion or by modulating peptide substances or neurotransmitters higher up in the hypothalamus. Gonadal steroids may also modulate the effect of peptides or dopamine at the level of the lactotrope. Prolactin's major role in the female rat is one of milk production post - partum, nurturing the young. It probably also has other physiological functions and may play a part in the menstrual cycle although this is controversial. Certainly, pulsatile secretion of prolactin during the menstrual cycle is well established and in the luteal phase this is concomitant with the secretion of luteinizing hormone. Theories explaining the synchronous surges seen during this phase of the menstrual cycle have been proposed and GnRH has been implicated in the genesis of the concordance of these secretory spikes. Using a potent GnRH antagonist an experiment was undertaken to establish the role of GnRH by blocking this hypothalamic peptide and observing the effect that this had on luteinizing hormone, prolactin and follicle stimulating hormone. In the first part of the thesis the control of prolactin secretion is reviewed. In the following section, an experiment was performed using a potent GnRH antagonist. A dose response curve was established for the antagonist action on LH. Then a twice maximum dose of this peptide was administered to three subjects in the midluteal phase of the menstrual cycle and the response of LH, prolactin and FSH was measured. The results indicate that although the GnRH antagonist significantly blocked LH secretory peaks, this action was not observed for either prolactin or FSH. This result is perhaps at variance with previous data which suggested that GnRH was responsible for concordant secretory spikes of LH and prolactin in the midluteal phase of the menstrual cycle.
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De, Villiers Charon. "The effect of gonadotropin-releasing hormones (GnRH) I & II on sperm motility and acrosome status of the Vervet monkey (Chlorocebus aethiops) in vitro." Thesis, University of the Western Cape, 2006. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_9134_1253841818.

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<p>Gonadotropin Releasing Hormone (GnRH) is a hypothalmic decapeptide, which regulates mammalian gonadotropin secretions by binding to specific, high affinity receptors in the pituitary. Two forms of GnRH (GnRH I and GnRH II) are expressed in the brain of human and some primates. Even though primates have been used extensively in a variety of investigations in relation to the role of GnRH in reproduction, there is no evidence of any research to investigate the direct effect of GnRH on primate sperm.</p>
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Jeanne, Fabian. "Evοlutiοns des systèmes GΝRΗ et des hοrmοnes glycοprοtéiques dans les cοntrôles endοcrine et paracrine de la spermatοgénèse chez la rοussette, Scyliοrhinus canicula". Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMC225.

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La spermatogenèse est un processus hautement spécialisé de prolifération et de différenciation cellulaire conduisant à la production de spermatozoïdes haploïdes à partir de cellules souches spermatogoniales diploïdes. Chez les Gnathostomes, les fonctions testiculaires sont principalement contrôlées de façon endocrine par l’axe hypothalamo-hypophyso-gonadique (HHG) impliquant notamment les GnRHs hypothalamiques et les hormones gonadotropes, FSH et LH, dont l’émergence s’est produite à la racine des Vertébrés cartilagineux. De plus, des fonctions paracrines des GnRHs et de la thyrostimuline ont été explorées au niveau gonadique chez des Vertébrés osseux. L’objet de cette thèse était de caractériser les régulations endocrines et paracrines de la spermatogenèse médiées par les GnRHs et les hormones gonadotropes chez un modèle Élasmobranche, la roussette Scyliorhinus canicula. Ce travail a été étendu à la caractérisation de GPA2 et GPB5, constituant la thyrostimuline, qui correspondent aux orthologues des ancêtres moléculaires des sous-unités des hormones glycoprotéiques. Dans ce travail, l’évolution du protéome testiculaire au cours de la spermatogenèse de S. canicula a été décrite, les neuropeptides GnRHs, les hormones glycoprotéiques FSH, LH, TSH, GPA2 et GPB5, et leurs récepteurs associés ont fait l’objet d’analyses in silico et d’expressions dans différents tissus avec un focus au cours de la spermatogenèse. Il a été observé une expression à tous les stades de la spermatogenèse de fshr, lhr et des récepteurs aux GnRHs au niveau germinale et sertolien, de tshr et gpb5 au niveau sertolien et de gpa2 au niveau germinal, avec des abondances plus importantes associées aux stades spermatides. Ce travail a été complété par des tests fonctionnels in vitro qui ont montré que FSHR pouvait être activé par FSH et LH, LHR uniquement par LH, et que GPB5-GPA2 pouvait activer les trois récepteurs FSHR, LHR et TSHR, suggérant ainsi un rôle paracrine de la thyrostimuline au niveau testiculaire. L’ensemble de ce travail permet de proposer un modèle de régulation de la spermatogenèse chez les Élasmobranches qui associe des hormones endocrines, avec les GnRHs et gonadotropines circulantes, et des hormones paracrines, avec GPA2, GPB5 et les stéroïdes. Ce modèle apparaît cohérent et intermédiaire dans l’évolution des systèmes régulateurs de la spermatogenèse qui seraient passés d’une régulation paracrine prépondérante chez les Bilatériens non-Vertébrés à une régulation endocrine prépondérante chez les Vertébrés osseux avec la mise en place de l’axe hypothalamo-hypophyso-gonadique<br>Spermatogenesis is a highly specialized process of cell proliferation and differentiation leading to the production of haploid spermatozoa from diploid spermatogonial stem cells. In Gnathostomes, testicular functions are mainly controlled by the endocrine hypothalamic-pituitary-gonadal (HHG) axis, involving hypothalamic GnRHs and the gonadotropic hormones FSH and LH, which emerged at the root of cartilaginous vertebrates. In addition, paracrine functions of GnRHs and thyrostimulin have been explored at the gonadic level in bony vertebrates. The aim of this thesis was to characterize the endocrine and paracrine regulation of spermatogenesis exerted by GnRHs and gonadotropic hormones in an Elasmobranch model, the catshark Scyliorhinus canicula. This work has been extended to the characterization of GPA2 and GPB5, constituting thyrostimulin, which correspond to orthologs of the molecular ancestors of glycoprotein hormone subunits. In this work, the evolution of the testicular proteome during spermatogenesis in S. canicula was described, and the neuropeptides GnRHs, the glycoprotein hormones FSH, LH, TSH, GPA2 and GPB5, as well as their associated receptors were studied by in silico and expression analyses in different tissues, with a focus on spermatogenesis. Expressions were observed at all stages of spermatogenesis for fshr, lhr and GnRH receptors associated at germinal and sertolian levels, for tshr and gpb5 at sertolian level and for gpa2 at germinal level, with higher abundances associated with spermatid stages. This work was complemented by in vitro functional tests which showed that FSHR could be activated by FSH and LH, LHR only by LH, and that GPB5-GPA2 could activate all three receptors FSHR, LHR and TSHR, suggesting a paracrine role for thyrostimulin at the testicular level. Taken together, this work proposes a model for the regulation of spermatogenesis in Elasmobranchs that combines endocrine hormones, with circulating GnRHs and gonadotropins, and paracrine hormones, with GPA2, GPB5 and steroids. This model appears consistent and intermediate in the evolution of spermatogenesis regulating systems, which has shift from predominantly paracrine regulation in non-vertebrate bilaterians to predominantly endocrine regulation in bony vertebrates, with the establishment of the hypothalamic-pituitary-gonadal axis
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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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12

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 G<sub>q</sub>-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/Ca<sup>2+ </sup>pathway activation by GnRH is described. GnRH was found to activate NFAT, a potential effecter of the non-canonical Wnt/Ca<sup>2+</sup> pathway. GnRH-induced NFAT activation was found to be dependent on important mediators of the non-classical Wnt/Ca<sup>2+</sup> pathway, including G<sub>q</sub>, Ca<sup>2+</sup>, 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/Ca<sup>2+</sup> 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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13

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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14

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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15

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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16

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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17

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. <i>In situ </i>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-Ca<sup>2+</sup>/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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18

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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19

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.

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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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20

Wibullaksanakul, Sunee. "Regulation of gonadotropin releasing hormone (GnRH) secretion : in-vitro studies in the male rat." Thesis, The University of Sydney, 1992. https://hdl.handle.net/2123/26487.

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The study described in this thesis was carried out between 1986—1990 while the author was a postgraduate candidate at The University of Sydney, and in receipt of a scholarship from the Australian International Development Assistance Bureau (AIDAB), Department of Foreign Affairs and Trade. The author would like to thank AIDAB for its financial support. During this time, all experimental work and data analysis was carried out by the author, with excellent technical assistance from Mrs Jennifer Spaliviero and Miss Elsa Kidston. Experimental work involving animals was approved by the University of Sydney Animal Ethics Review Committee. Matters of design and interpretation were closely supervised by Associate Professor David J Handelsman, whose invaluable advice the author wishes to acknowledge. This thesis has been arranged into six related chapters. The first section is a literature review. This section outlines the current state of knowledge concerning general~ aspects of gonadotropin—releasing hormone (GnRH) function, regulatory mechanisms of hypothalamic GnRH secretion, and the methodology suitable for investigation of the regulatory mechanisms of GnRH secretion from the medial basal hypothalamus (MBH) of adult male rats. Both systems are compared for features of methodological integrity, including stability of baseline GnRH release and technical limitations or artefacts. In the third part of this work, these in-vitro methods are applied to examine the effect of castration on GnRH secretion, the results of which are discussed in chapter three. The fourth section of this project concerns the effects of steroids, opioids and noradrenergic signals on GnRH secretion from MBH of adult male rats. In the fifth section of this project, the effect of experimental uremia as a model disease on GnRH secretion is addressed. The last chapter of this project is a summary and discussion. Since each chapter is discussed in detail, the final section is an overview of the content of previous chapters.
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21

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.<br>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.<br>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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22

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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23

Stavrou, Emmanouil. "Regulation of FOXO transcription factors by gonadotropin-releasing hormone." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5686.

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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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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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25

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.<br>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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26

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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27

Miller, Nichol L. G. "Transcriptional control of the gonadotropin-releasing hormone gene in development." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC IP addresses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3296836.

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Thesis (Ph. D.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed June 3, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 113-126).
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28

Ford, H. "Regulation of gonadotropin-releasing hormone neurons by the neurotransmitter glutamate." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599110.

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The neurotransmitter glutamate has been proposed as a potential regulator of the onset of puberty, due to its actions on the neurons within the hypothalamus which release gonadotropin-releasing hormone (GnRH). The studies in this thesis have investigated this hypothesis, by determining the effects of glutamate on GnRH gene expression and the effects of manipulating the ability of glutamate to signal to the GnRH neurons via N-methyl-D-aspartate (NMDA)-type glutamate receptors. Studies in this thesis utilised two transgenic mouse lines with mutations in the common NR1 subunit of the NMDA receptor. One line was to complete knockout for this gene (<I>NRI<SUP>-/-</SUP></I>), and the other contained a point mutation which rendered it dysfunctional (<I>NRI<SUP>Q/Q</SUP></I>). Both lines were shown to possess a normal number of GnRH perikarya, in a normal distribution. The approach of semi-quantitative <I>in situ</I> hybridisation was used to demonstrate that GnRH mRNA levels increased with developmental age in the mouse. The neurotransmitter glutamate was shown to be involved in the endogenous regulation of GnRH mRNA levels in the mouse, and is proposed as a potential regulator of the developmental increase. Glutamatergic stimulation had no effect on GnRH mRNA within <I>NRI<SUP>-/-</SUP></I> animals, showing that these effects are likely to be mediated by NMDA receptors. The functional capability of the GnRH neurons of <I>NRI<SUP>Q/Q</SUP></I> animals was tested by transplanting them into the brain of the infertile, GnRH-deficient, hypogonadal (<I>hpg</I>) mouse. Grafted GnRH neurons from wild-type and <I>NRI<SUP>Q/Q</SUP></I> animals were found to innervate the median eminence normally, and were capable of inducing increased testis size, increased serum testosterone and the onset of spermatogenesis in <I>hpg</I> male hosts.
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29

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.

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Thesis (MSc)--University of Stellenbosch, 2007.<br>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.<br>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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30

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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31

Clarkson, Jenny, and n/a. "Activation of Gonadotropin-releasing hormone neurons by Kisspeptin in the mouse." University of Otago. Department of Physiology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20081208.114143.

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The gonadotropin-releasing hormone (GnRH) neurons are the final output neurons of a complex neuronal network that controls fertility in all mammals. The GnRH neurons reside in a scattered continuum throughout the anterior hypothalamus. The majority of GnRH neurons project an axon to the median eminence where GnRH is secreted into the hypophyseal-pituitary portal vessels from whence it travels to the anterior pituitary gland. GnRH acts on the gonadotrophs of the anterior pituitary gland to cause the secretion of luteinising hormone (LH) and follicle stimulating hormone (FSH) into the peripheral circulation. LH and FSH act on the gonads to control gametogenesis and steroidogenesis. This thesis focuses on two unanswered questions in reproductive neurobiology that are fundamental to fertility 1) how the GnRH neurons become activated at puberty to produce patterned GnRH secretion and 2) the nature of the positive feedback mechanism that drives the preovulatory GnRH and LH surges. Recently, a novel neuropeptide called kisspeptin and its G-protein coupled receptor GPR-54 were found to be essential for pubertal activation of GnRH neurons, with GPR-54 mutation or deletion resulting in failed puberty and infertility in humans and mice. In addition, kisspeptin administration potently stimulates GnRH neuron-mediated gonadotropin secretion and advances the onset of pubertal maturation suggesting an important role for kisspeptin in the activation and perhaps post-pubertal modulation of GnRH neurons. In this thesis I have used immunocytochemical, whole animal manipulations and knockout mouse approaches to investigate the role of kisspeptin in both the activation of GnRH neurons at puberty and in the estrogen positive feedback mechanism in the mouse. I have demonstrated that kisspeptin neurons are located principally in the rostral periventricular area of the third ventricle (RP3V) and the arcuate nucleus (ARN), which are both known to be important areas for the modulation of GnRH neuronal activity. Kisspeptin fibres are found in abundance throughout the hypothalamus, but of particular interest are the kisspeptin fibres found in close apposition with a subset of GnRH neurons in the rostral preoptic area (rPOA). The kisspeptin neurons in the RP3V are sexually dimorphic with up to ten times more neurons in the female than the male. The number of kisspeptin neurons in the RP3V increases throughout pubertal development reaching adult levels at the time of puberty in both males and females. In concert with the increase in the number of kisspeptin neurons in the RP3V there is an increase in the percentage of GnRH neurons in the rPOA which exhibited a close apposition with a kisspeptin fibre indicating that kisspeptin neurons may target GnRH neurons to activate them at puberty. Additionally, I demonstrate that the increase in the number of neurons in the RP3V of the female mouse approaching puberty is driven by estrogen secreted from the ovary. A significant number of kisspeptin neurons in the RP3V were shown to express tyrosine hydroxylase (TH). The number and percentage of kisspeptin cells colocalised with TH cells in the RP3V did not change throughout the estrous cycle. Some colocalisation of kisspeptin and TH was observed at terminal appositions with GnRH neurons in the rPOA, though the magnitude of colocalisation also did not change throughout the estrous cycle. I demonstrate that RP3V kisspeptin neurons are a critical part of the estrogen positive feedback mechanism which drives the preovulatory GnRH and LH surges. Kisspeptin neurons in the RP3V express steroid receptors and are activated by estrogen positive feedback. Loss of kisspeptin-GPR-54 signalling prevents the GnRH neurons from being activated by estrogen positive feedback indicating that the RP3V kisspeptin neurons not only contribute to the estrogen positive feedback mechanism, but are a critical component of the mechanism. The results of these studies demonstrate that kisspeptin is an integral component in both the activation of GnRH neurons at puberty and in the estrogen positive feedback mechanism which drives the preovulatory GnRH and LH surges. Therefore, kisspeptin plays an important role in the neuroendocrine control of reproduction in the mouse.
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32

Cheung, Wai-ting, and 張慧婷. "Role of gonadotropin-releasing hormone of metastatic potential of ovarian cancer cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41634184.

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33

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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34

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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35

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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36

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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37

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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38

戚賜聰 and Chi-chung Stanley Chik. "Characterization of two chicken gonadotropin releasing hormone-II genes in goldfish, Carassius Auratus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31220629.

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39

Morton, Stephanie. "Effects of continuous treatment with gonadotropin-releasing hormone during the anovulatory season on gonadotropin secretion, follicular dynamics and ovulation in the mare." Texas A&M University, 2004. http://hdl.handle.net/1969.1/1551.

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Objectives were to determine if low-dose, continuous infusion of GnRH from Fall to Spring, would prevent seasonal anovulation in mares. Twenty Quarter Horse mares, ages 18 mo to 24 yrs, were stratified by age and body condition score and assigned randomly to either a saline control (n = 9) or GnRH (n = 11) treatment group. Treatments were instituted between September 23 and October 9, 2002. Gonadotropinreleasing hormone was delivered in 0.9% physiological saline via Alzet osmotic minipumps (Model 2004) placed sc at the base of the neck, with Silastic sham pumps placed in control mares. Pumps were inserted on day 3 following ovulation or during the follicular phase if ovulation had not occurred. Delivery rate of GnRH was 2.5 ug/h (60 ug/d) for the first 60 d, followed by 5.0 ug/h (120 ug/d) thereafter, with all pumps replaced every 30 d. By December 1, all mares had become anovulatory and remained anovulatory until February. Mean serum concentrations of LH were not affected by treatment in anovulatory mares. In contrast, control mares that exhibited ovulatory cycles after treatment onset had higher (P < 0.05) mean concentrations of LH during all phases of the estrous cycle except diestrus. Mean serum concentrations of FSH were not affected by treatment, but were lower (P < 0.05) from November though January relative to all other months in anovulatory mares. Interovulatory intervals in mares that cycled temporarily did not differ between groups. Ovulatory control mares had slightly larger (P < 0.10) follicles overall than GnRH-treated mares; however, ovulatory follicle diameters for control and GnRH-treated mares did not differ. Ovulatory control mares had higher (P < 0.10) mean concentrations of progesterone during metestrus and late diestrus. In a subgroup of control (n =5) and GnRH-treated (n = 5) mares, total releasable pools of LH in response to 1 mg GnRH did not differ between groups. Ovulation resumed in 3 control and 3 GnRH-treated mares by March 30. Results indicate that continuous infusion of native GnRH at the doses employed herein is not sufficient to maintain ovulatory cycles during the anovulatory season.
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40

Mirhadi, Eila. "Regulation of gonadotropin-releasing hormone (GnRH) transcript production in the goldfish ovary." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ38601.pdf.

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41

Ronacher, Katharina. "Internalisation of the type II gonadotropin-releasing hormone receptor of marmoset monkey." Doctoral thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/8599.

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Bibliography: leaves 102-124.<br>The mammalian type II GnRH receptor has a C-terminal tail unlike the mammalian type I GnRH receptor, which uniquely lacks the cytoptasmic C- terminal domain. lnternalisation of a mammalian type ll GnRH receptor has never been investigated, therefore this thesis studies the internalisation pathway of the type ll GnRH receptor. As the C-terminal tail mediates rapid internalisation of many G protein-coupled receptors this research investigates the functional role of the C-terminal tail and intracellular loop in receptor internalisation. The internalisation pathway of the type ll GnRH receptor in COS-1 cells was investigated by co expressing dominant negative mutants and wild- type constructs of G protein-coupled receptor kinases (GRKs), dynamin-1 and β-arrestin 1 and 2 with the type II GnRH receptor. The results show that internatisation of the receptor requires GRK 2 and dynamin but does not require β-arrestin 1 and 2. Furthermore, inhibitors to both the caveolae pathway as well as the clathrin coated vesicle endocytosis abolished receptor internalisation indicating that both structures are involved in internalisation of the receptor. Even though in COS-1 cells the type ll GnRH receptor internatises in a β-arrestin independent manner, internalisation of this receptor can be enhanced by over-expression of wild type β-arrestin. This indicates that the type ll GnRH receptor is able to utilise a β-arrestin mediated internaltsation pathway if high levels of β-arrestin are present in the cell. The mammalian type ll GnRH receptor internalises with enhanced rate and extent compared to the tail-less human type I GHRH receptor. The role of the C-terminal tail of the type ll GnRH receptor in internalisation was investigated by measuring internalisation of C-terminally truncated mutants. It was found that the region between Gly 343 and Ser 335 within the C-terminal domain is important for receptor internalisation. Substitution of putative phosphorylation sites within this region revealed that Ser 338 and Ser 339 are critical for rapid receptor internalisation. Furthermore a serine residue in intracellular loop three (Ser 251) was shown to play a role in signalling as well as in internalisation. Since dominant negative GRK 2 could not inhibit internalisation of a mutant lacking all three serine residues, but could reduce internalisation of the wild-type receptor, we suggest that Ser 251, 338 and 339 are target of phosphorylation by GRK. However these phosphorylation sites as well as the C-terminal tail are not necessary for β-arrestin dependent internalisation. Taken together this thesis elucidates the internalisation pathway of a mammalian type lI GnRH receptor and identified residues within the C-terminal tail and intracellular loop three that are critical for rapid internalisation.
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Pithey, Anne Louise. "Autocrine regulation of gonadotropin-releasing hormone in immortalized hypothalamic GT1-7 neurons." Master's thesis, University of Cape Town, 1994. http://hdl.handle.net/11427/27030.

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The existence of an ultrashort feedback mechanism regulating GnRH secretion has been supported from in vivo and in vitro studies. However, the complex synaptic connections of GnRH neurons with other neural elements made it difficult to determine whether the regulation was mediated by direct actions on the GnRH neurons or through actions on other interneurons. The recent development of the GnRH-secreting neuronal cell line, GT1, provided a model system for the study of neural regulation of a pure population of GnRH neurons. The present studies utilized GT1 -7 cells to investigate whether GnRH (at the level of the nerve terminal) influences the control of its own release. Preliminary studies determined the presence of GnRH mRNA in GT1-7 cells and established a cell culture system for the analysis of secretagogue-induced GnRH release. In this system GnRH release was shown to be spontaneous and was enhanced by the addition of K⁺, L-GLU, forskolin and PMA. Furthermore, K⁺- and forskolin-induced GnRH release was dependent on extracellular Ca²⁺. For the analysis of an ultrashort feedback mechanism, GT1-7 cells were cultured in 6-well plates to near confluence and then incubated in serum-free medium in the presence (1 nM- 1 μM) or absence of GnRH antagonist, Ant 27. Basal, K⁺-and forskolin-induced secretion of GnRH was monitored with antiserum 1076 which does not cross-react with Ant 27 at> 1 μM. Ant 27 treatment increased basal, K⁺- and forskolin-stimulated GnRH release in a dose-dependent manner. Total content was unaffected by 18 h treatment of GT1-7 cells with Ant 27. This suggests that the effects of Ant 27 are at the level of release and not biosynthesis. The presence of GnRH binding sites in the cells was demonstrated with ¹²⁵I-GnRH analog. These findings support the concept that GnRH, acting via autoreceptors, negatively controls its own release.
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Hutchinson, Emerentia. "The cloning of novel gonadotropin-releasing hormone receptors by polymerase chain reaction." Master's thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26968.

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Gonadotropin-releasing hormone (GnRH), a central regulator of reproductive function in all vertebrates, exerts its effects via binding to the GnRH receptor (GnRHR) in the pituitary gonadotrophs. The GnRHR is a member of the G-protein coupled receptor (GPCR) superfarnily. A second form of the GnRHR (type II), other than the pituitary gonadotrope GnRHR (type I) has been proposed to exist and to play a role other than the classical endocrine role of the pituitary GnRHR. Elucidation of amino acid residues of the GnRHR that are crucial for ligand binding, activation of the receptor, and coupling to the G-protein, is important in understanding structure-function relationships towards the design of drugs for therapeutic intervention. Such information can often be deduced by a comparison between conserved and non-conserved amino acid residues of GnRHRs from different species. At the start of this project no non-mammalian or invertebrate, and only some of the eutherian mammalian type I GnRHRs had been cloned. The aim of this project was to clone novel GnRHRs, i.e. type I and type II GnRHRs from redbait and mole and type II mouse and human GnRHRs using polymerase chain reaction (PCR) strategies. PCR was performed with degenerate primers designed to human type I GnRHR to areas that are not conserved between GPCRs in general, but are conserved between mammalian GnRHRs.
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44

MacConell, Leigh Anne. "The regulation of gonadotropin-releasing hormone biosynthesis and release by activin A /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9904817.

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45

Kelley, Carolyn Griffith. "Neuron-specific transcriptional activators directing expression 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, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9984304.

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46

Givens, Marjory L. "Molecular mechanisms promoting neuron-restricted expression 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, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3129941.

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47

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.<br>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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48

Lee, King-yiu. "Molecular cloning and characterization of gonadotropin-releasing hormone receptors in the black seabream (Mylio macrocephalus)." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22823876.

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49

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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Made available in DSpace on 2016-02-05T18:29:24Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-05-29. Added 1 bitstream(s) on 2016-02-05T18:33:27Z : No. of bitstreams: 1 000854973_20161205.pdf: 410109 bytes, checksum: 5ceaa1852fc805e9d99744c37a96f7bb (MD5) Bitstreams deleted on 2016-12-06T15:11:22Z: 000854973_20161205.pdf,. Added 1 bitstream(s) on 2016-12-06T15:12:04Z : No. of bitstreams: 1 000854973.pdf: 2773395 bytes, checksum: daf1de70009034e8b87b75a4cc4b7610 (MD5)<br>Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)<br>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...<br>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 ...<br>FAPESP: 2014/02481-9
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50

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 Nakaghi<br>Coorientador: Rafael Henrique Nóbrega<br>Banca: Elisabeth Criscuolo Urbinati<br>Banca: Matias Pandolfi<br>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...<br>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 ...<br>Mestre
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