Academic literature on the topic 'Urocortine'
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Journal articles on the topic "Urocortine"
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Takahashi, Kazuhiro. "Distribution of Urocortins and Corticotropin-Releasing Factor Receptors in the Cardiovascular System." International Journal of Endocrinology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/395284.
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Urocortins are human homologues of urotensin I, a fish corticotropin-releasing-factor- (CRF-) like peptide secreted from the urophysis. There are three urocortins: urocortin 1, urocortin 2, and urocortin 3 in mammals. We have shown that urocortin 1 and urocortin 3 are endogenously synthesized in the myocardial cells of human heart and may act on CRF type 2 receptor (CRFR2) expressed in the heart. Expression levels of urocortin 1 in the heart and plasma urocortin 1 levels are elevated in patients with heart failure. Recent studies have shown that urocortins have various biological actions in the cardiovascular system, such as a vasodilator action, a positive inotropic action, a cardioprotective action against ischemia/reperfusion injury, and suppressive actions against the renin angiotensin system and the sympathetic nervous system. Urocortins and CRFR2 may therefore be a potential therapeutic target for cardiovascular diseases, such as congestive heart failure, hypertension, and myocardial infarction.
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Boorse, Graham C., Erica J. Crespi, Frank M. Dautzenberg, and Robert J. Denver. "Urocortins of the South African Clawed Frog, Xenopus laevis: Conservation of Structure and Function in Tetrapod Evolution." Endocrinology 146, no. 11 (November 1, 2005): 4851–60. http://dx.doi.org/10.1210/en.2005-0497.
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Several corticotropin-releasing factor (CRF) family genes have been identified in vertebrates. Mammals have four paralogous genes that encode CRF or the urocortins 1, 2, and 3. In teleost fishes, a CRF, urotensin I (a fish ortholog of mammalian urocortin 1) and urocortin 3 have been identified, suggesting that at least three of the four mammalian lineages arose in a common ancestor of modern bony fishes and tetrapods. Here we report the isolation of genes orthologous to mammalian urocortin 1 and urocortin 3 from the South African clawed frog, Xenopus laevis. We characterize the pharmacology of the frog peptides and show that X. laevis urocortin 1 binds to and activates the frog CRF1 and CRF2 receptors at picomolar concentrations. Similar to mammals, frog urocortin 3 is selective for the CRF2 receptor. Only frog urocortin 1 binds to the CRF-binding protein, although with significantly lower affinity than frog CRF. Both urocortin genes are expressed in brain, pituitary, heart, and kidney of juvenile frogs; urocortin 1 is also expressed in skin. We also identified novel urocortin sequences in the genomes of pufferfish, zebrafish, chicken, and dog. Phylogenetic analysis supports the view that four paralogous lineages of CRF-like peptides arose before the divergence of the actinopterygian and sarcopterygian fishes. Our findings show that the functional relationships among CRF ligands and binding proteins, and their anorexigenic actions mediated by the CRF2 receptor, arose early in vertebrate evolution.
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Neufeld-Cohen, A., M. M. Tsoory, A. K. Evans, D. Getselter, S. Gil, C. A. Lowry, W. W. Vale, and A. Chen. "A triple urocortin knockout mouse model reveals an essential role for urocortins in stress recovery." Proceedings of the National Academy of Sciences 107, no. 44 (October 11, 2010): 19020–25. http://dx.doi.org/10.1073/pnas.1013761107.
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Hasdemir, Burcu, Shilpi Mahajan, Juan Oses-Prieto, Shreya Chand, Michael Woolley, Alma Burlingame, Dimitris K. Grammatopoulos, and Aditi Bhargava. "Actin cytoskeleton–dependent regulation of corticotropin-releasing factor receptor heteromers." Molecular Biology of the Cell 28, no. 18 (September 2017): 2386–99. http://dx.doi.org/10.1091/mbc.e16-11-0778.
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Stress responses are highly nuanced and variable, but how this diversity is achieved by modulating receptor function is largely unknown. Corticotropin-releasing factor receptors (CRFRs), class B G protein–coupled receptors, are pivotal in mediating stress responses. Here we show that the two known CRFRs interact to form heteromeric complexes in HEK293 cells coexpressing both CRFRs and in vivo in mouse pancreas. Coimmunoprecipitation and mass spectrometry confirmed the presence of both CRF1R and CRF2βR, along with actin in these heteromeric complexes. Inhibition of actin filament polymerization prevented the transport of CRF2βR to the cell surface but had no effect on CRF1R. Transport of CRF1R when coexpressed with CRF2βR became actin dependent. Simultaneous stimulation of cells coexpressing CRF1R+CRF2βR with their respective high-affinity agonists, CRF+urocortin2, resulted in approximately twofold increases in peak Ca2+responses, whereas stimulation with urocortin1 that binds both receptors with 10-fold higher affinity did not. The ability of CRFRs to form heteromeric complexes in association with regulatory proteins is one mechanism to achieve diverse and nuanced function.
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Tezval, Hossein, Axel S. Merseburger, Markus A. Kuczyk, Christoph von Klot, and Juergen Serth. "Quantitative comparison of mRNA level of corticotropin- releasing factor peptide family in normal kidney and corresponding clear cell renal cell carcinoma specimens." Journal of Clinical Oncology 33, no. 7_suppl (March 1, 2015): 466. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.466.
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466 Background: Urocortin (Ucn), a 40 amino acid peptide, belongs to the corticotropin releasing factor (CRF) family and exerts its actions mainly in the periphery through activation of two CRF receptors (CRFRs), CRFR1 and CRFR2 and a binding protein (CRFBP/CRHBP). Both receptors are G-protein coupled and binding of Ucn leads to activation of cAMP-dependent protein kinases via elevation of cAMP levels. Ucn and Urocortin III (UcnIII) are involved in conditions such as regulation of local inflammation, angiogenesis, and inhibition of proliferation. Suppression of neovascularization and inhibition of tumor cell cycling by Urocortins is modulated through CRFRs. Activation of CRFRs by e.g. Ucn inhibits angiogenesis via reduction of vascular endothelial growth factor (VEGF) and suppresses the cell proliferation. Here we characterized the whole CRF family on mRNA levels quantitatively comparing the normal and clear cell carcinoma of the kidney (ccRCC). Methods: In this study we measured the mRNA level of Ucn, UcnIII, CRFR1, CRFR2 and CRHBP in 78 RCC samples and paired histologically normal appearing tissues using quantitative PCR. Statistical analyses were carried out using univariate logistic regression analysis. Results: We found tumour specific down regulation of mRNA expression of UcnIII, CRFR1, CRFR2 and CRHBP in samples of RCCs with clear cell histology compared to paired normal tissues (P<0.01 for all targets). Only Ucn did not show any expression difference between two groups (p=0.17). Conclusions: For the first time we showed the expression profile of the whole CRF peptide family in ccRCC compared to normal kidney on mRNA level. Our data underlines the malfunction of this actually strong protective and anticancer system in renal malignancy and shows the involvement of CRF system in carcinogenesis in kidney. More studies are necessary to find out the detailed roles of the CRF system in renal carcinoma.
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Gourcerol, G., L. Wang, Y. H. Wang, M. Million, and Y. Taché. "Urocortins and Cholecystokinin-8 Act Synergistically to Increase Satiation in Lean But Not Obese Mice: Involvement of Corticotropin-Releasing Factor Receptor-2 Pathway." Endocrinology 148, no. 12 (December 1, 2007): 6115–23. http://dx.doi.org/10.1210/en.2007-0678.
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Interactions between gastrointestinal signals are a part of integrated systems regulating food intake (FI). We investigated whether cholecystokinin (CCK)-8 and urocortin systems potentiate each other to inhibit FI and gastric emptying (GE) in fasted mice. Urocortin 1 and urocortin 2 (1 μg/kg) were injected ip alone or with CCK (3 μg/kg) in lean, diet-induced obese (DIO) or corticotropin-releasing factor receptor-2 (CRF2)-deficient mice. Gastric vagal afferent activity was recorded from a rat stomach-vagus in vitro preparation. When injected separately, urocortin 1, urocortin 2, or CCK did not modify the 4-h cumulative FI in lean mice. However, CCK plus urocortin 1 or CCK plus urocortin 2 decreased significantly the 4-h FI by 39 and 27%, respectively, compared with the vehicle + vehicle group in lean mice but not in DIO mice. Likewise, CCK-urocortin-1 delayed GE in lean but not DIO mice, whereas either peptide injected alone at the same dose had no effect. CCK-urocortin 2 suppression of FI was observed in wild-type but not CRF2-deficient mice. Gastric vagal afferent activity was increased by intragastric artery injection of urocortin 2 after CCK at a subthreshold dose, and the response was reversed by devazepide. These data establish a peripheral synergistic interaction between CCK and urocortin 1 or urocortin 2 to suppress FI and GE through CRF2 receptor in lean mice that may involve CCK modulation of gastric vagal afferent responsiveness to urocortin 2. Such synergy is lost in DIO mice, suggesting a resistance to the satiety signaling that may contribute to maintain obesity.
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Kihara, Naoki, Masaki Fujimura, Ikuo Yamamoto, Etsuro Itoh, Akio Inui, and Mineko Fujimiya. "Effects of central and peripheral urocortin on fed and fasted gastroduodenal motor activity in conscious rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 3 (March 1, 2001): G406—G419. http://dx.doi.org/10.1152/ajpgi.2001.280.3.g406.
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Since few previous studies have examined the effects of urocortin on physiological fed and fasted gastrointestinal motility, we administered urocortin intracerebroventricularly (icv) or intravenously (iv) in freely moving conscious rats and examined the changes in antral and duodenal motility. Icv and iv injection of urocortin disrupted fasted motor patterns of gastroduodenal motility, which were replaced by fed-like motor patterns. When urocortin was given icv and iv in the fed state, the motor activity remained like the fed patterns but % motor index (%MI) was decreased in the antrum and increased in the duodenum. Increase in the %MI in the duodenum induced by urocortin was shown as a nonpropagated event, since the transit of nonnutrient contents in the duodenum was decreased by icv and iv injection of urocortin. Changes in the gastroduodenal motility induced by icv injection of urocortin were abolished in animals with truncal vagotomy but not altered in animals with mechanical sympathectomy, suggesting that the vagal pathway may mediate the central action of urocortin. Neither urocortin antiserum nor α-helical CRF-(9–41) affected fed and fasted gastroduodenal motility, suggesting that endogenous urocortin is not involved in regulation of basal gastroduodenal motility.
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Holloway, Alison C., David C. Howe, Gabriel Chan, Vicki L. Clifton, Roger Smith, and John R. G. Challis. "Urocortin: a mechanism for the sustained activation of the HPA axis in the late-gestation ovine fetus?" American Journal of Physiology-Endocrinology and Metabolism 283, no. 1 (July 1, 2002): E165—E171. http://dx.doi.org/10.1152/ajpendo.00497.2001.
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We hypothesized that urocortin might be produced in the pituitary of the late-gestation ovine fetus in a manner that could contribute to the regulation of ACTH output. We used in situ hybridization and immunohistochemistry to identify urocortin mRNA and protein in late-gestation fetal pituitary tissue. Levels of urocortin mRNA rose during late gestation and were associated temporally with rising concentrations of pituitary proopiomelanocortin (POMC) mRNA. Urocortin was localized both to cells expressing ACTH and to non-ACTH cells by use of dual immunofluorescence histochemistry. Transfection of pituitary cultures with urocortin antisense probe reduced ACTH output, whereas added urocortin stimulated ACTH output from cultured pituitary cells. Cortisol infusion for 96 h in chronically catheterized late-gestation fetal sheep significantly stimulated levels of pituitary urocortin mRNA. We conclude that urocortin is expressed in the ovine fetal pituitary and localizes with, and can stimulate output of, ACTH. Regulation of urocortin by cortisol suggests a mechanism to override negative feedback and sustain feedforward of fetal hypothalamic-pituitary-adrenal function, leading to birth.
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Iino, Kazumi, Hironobu Sasano, Yutaka Oki, Noriaki Andoh, Ryong-Woon Shin, Tetsuyuki Kitamoto, Kazuhito Totsune, et al. "Urocortin Expression in Human Pituitary Gland and Pituitary Adenoma." Journal of Clinical Endocrinology & Metabolism 82, no. 11 (November 1, 1997): 3842–50. http://dx.doi.org/10.1210/jcem.82.11.4371.
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Urocortin is a recently identified neuropeptide of the CRF family in the mammalian brain, but its expression in human tissue has been little studied. In this study, we examined urocortin expression in human anterior pituitary gland and pituitary adenomas by RIA, high performance liquid chromatography, immunohistochemistry, messenger ribonucleic acid (mRNA) in situ hybridization, and reverse transcriptase-PCR. Immunoreactive urocortin concentrations in normal pituitary tissue extract were 103.25 ± 39.05 ng/g wet wt (mean ± sem; n = 4), and their levels were all significantly higher than those in other portions of central nervous system of the same subjects. High performance liquid chromatography analysis of human pituitary extract demonstrated a single peak corresponding to that of the expected chromatographic mobility of synthetic human urocortin-(1–40). Urocortin-immunoreactive cells were detected in the anterior pituitary gland. Neither urocortin-immunoreactive nerve fibers nor cells were detected in the posterior lobe. Immunostaining in serial mirror tissue sections revealed that 76.55 ± 3.06% of urocortin-immunoreactive cells expressed GH immunoreactivity, whereas 22.25 ± 3.02% and less than 1% of urocortin-immunoreactive cells expressed PRL and ACTH, respectively. mRNA hybridization signals of urocortin were also detected in urocortin-immunopositive pituitary cells. The reverse transcriptase-PCR analysis demonstrated a 145-bp RNA band corresponding to that of the expected length of urocortin in all cases of normal pituitary glands examined (n = 3). We also immunostained urocortin in 52 cases of human anterior pituitary adenomas, including GH-producing adenomas (n = 14), ACTH-producing adenomas (n = 13), PRL-producing adenomas (n = 11), and nonfunctioning hormonally inactive adenomas (n = 14). No urocortin immunoreactivity was detected in these adenoma cells, except for one case of GH-producing adenoma and one case of nonfunctioning adenoma. We also performed mRNA in situ hybridization in 27 adenomas. No hybridization signals were detected in these adenomas, except in two cases. The results described above indicated that urocortin is synthesized in human anterior pituitary cells and may play an important role in biological features of normal pituitary gland, possibly as an autocrine or a paracrine regulator.
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UZUKI, Miwa, Hironobu SASANO, Yasunari MURAMATSU, Kazuhito TOTSUNE, Kazuhiro TAKAHASHI, Yutaka OKI, Kazumi IINO, and Takashi SAWAI. "Urocortin in the synovial tissue of patients with rheumatoid arthritis." Clinical Science 100, no. 6 (April 25, 2001): 577–89. http://dx.doi.org/10.1042/cs1000577.
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Urocortin is a newly identified member of the corticotropin-releasing factor (CRF) neuropeptide family, and is known to be involved in the modulation of the inflammatory process. We examined the expression of urocortin, CRF and their receptors (CRF receptor; CRF-R) in the synovial tissue of patients with rheumatoid arthritis (RA) in order to study the possible biological roles of urocortin. Synovial tissues/fluids were obtained from 38 patients with RA, nine patients with osteoarthritis and four with trauma. We studied the concentration of urocortin in the synovial fluid using RIA, and the expression of urocortin in synovial tissue using immunohistochemistry, mRNA in situ hybridization and reverse transcriptase–PCR (RT-PCR). In addition, we examined the immunolocalization of CRF and the expression of CRF-R1, -R2-α and -R2-β mRNAs utilizing RT-PCR in these synovial tissues. Urocortin concentrations in synovial fluid were higher in RA patients (79.8±154 pg/ml) than in control patients (12.3±4.8 pg/ml; P ≤ 0.05). Urocortin immunoreactivity and mRNA signals were both detected in synovial cells, lymphocytes, fibroblasts and macrophages. The number of urocortin-positive cells in the synovium was significantly higher in RA (73.1±32.1 cells per high-power field) than in control (18.4±10.4 cells per high-power field) patients. In addition, both urocortin immunoreactivity and mRNA signals in the synovium reached maximum levels in the active stage of RA inflammation. Moreover, the number of immunoreactive urocortin-positive cells was significantly correlated with the urocortin concentration in synovial fluid (r = 0.705; P < 0.001) and with histologically defined local inflammatory activity (r = 0.641; P < 0.001). The distribution and number of immunoreactive CRF-positive cells in synovial tissue were similar to those of urocortin-positive cells (r = 0.701; P < 0.001). Urocortin, CRF-R1 and CRF-R2-α mRNAs detected by RT-PCR were expressed in in the synovium of 10/10, 10/10 and 2/10 RA patients respectively, but CRF-R2-β was not expressed. Urocortin was actively synthesized in the synovium of RA patients. The present study suggests that urocortin may play an important role as an autocrine and/or paracrine regulator of synovial inflammation in RA.
Dissertations / Theses on the topic "Urocortine"
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Moraru, Arthur. "Les effets de l'urocortine 3 sur le bilan énergétique chez le rat." Thesis, Université Laval, 2007. http://www.theses.ulaval.ca/2007/24257/24257.pdf.
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Gourcerol, Guillaume. "Modulation peptidergique au cours de la stimulation électrique gastrique." Rouen, 2007. http://www.theses.fr/2007ROUES034.
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La stimulation électrique gastrique est une nouvelle thérapie améliorant les symptômes des patients gastroparétiques sans modifier la vidange gastrique. Dans ce travail, nous avons d’abord démontré que l’efficacité clinique de cette technique est indépendante de la vidange gastrique. Puis nous avons mis en évidence chez le rat que cette thérapie pouvait moduler l’activité des neurones à corticotropin-releasing factor hypothalamiques, et ce de manière indépendante de la voie vagale. La modulation du système nerveux central par la stimulation électrique gastrique peut recruter soit les afférences spinales, soit être secondaire à la libération des peptides gastriques dans la circulation. Parmi ceux-ci, la ghréline ainsi que les urocortines sont potentiellement impliquées, compte-tenu de leurs effets sur la motricité digestive et la prise alimentaire. A l’inverse, l’obestatine, codée par le gène de la ghréline, n’est probablement pas mise en jeu compte tenu de son absence d’effets sur ces paramètresGastric electrical stimulation is a new therapy to relief symptoms of gastroparetic patients without affecting gastric emptying. In the present work, we first evidence that clinical improvement during this therapy was unrelated to gastric emptying. We next demonstrated in rats that gastric electrical stimulation could modulate hypothalamic corticotropin-releasing factor producing neurons, the later being vagal-independent. Then, this technique is likely to modulate central nervous system either by recruiting spinal afferent or though the release of gastric peptides in the bloodstream. Among them, ghrelin and urocortins are susceptible to explain such effect since they display significant effects on gastric motility and food intake. On the other hand, obestatin, encoded by the ghrelin gene, ihas no effect on feeding and digestive and does not represent a good candidate
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Silva, Natalia Lautherbach Ennes da. "Os efeitos da urocortina 2 no metabolismo de proteínas em músculos esqueléticos de roedores." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17134/tde-22112018-084729/.
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A urocortina 2 (Ucn2) é um peptídeo que pertence à família dos fatores liberadores de corticotrofina (CRF) e, assim como seu receptor específico CRF2R? (corticotropin releasing factor receptor type 2?), encontram-se expressos no músculo esquelético. Embora tenha sido demonstrado que o tratamento sistêmico com Ucn2 seja capaz de induzir hipertrofia e prevenir a perda de massa muscular, nada se conhece acerca dos mecanismos moleculares através dos quais a Ucn2 desempenha suas ações biológicas. O principal objetivo deste trabalho foi investigar o mecanismo de ação da Ucn2 no músculo esquelético de roedores para o aparecimento da resposta hipertrófica e a possível participação das vias de sinalização Akt/mTOR, Akt/Foxo e ERK1/2 neste efeito anabólico. Para isto foi utilizado o modelo de transfecção in vivo da Ucn2 pelo método da eletroporação em músculos tibialis anterior de camundongos. Nestes músculos foram quantificados: 1) o estado de fosforilação de componentes efetores destas vias; 2) moléculas sinalizadoras da via autofágica; 3) a taxa de síntese proteica in vivo e 4) a expressão de genes relacionados à atrofia muscular (atrogenes). Outra metodologia utilizada para verificar o efeito direto da Ucn2 na musculatura esquelética foi a incubação in vitro de músculos soleus e EDL isolados de roedores com este peptídeo a fim de investigar a taxa de degradação proteica total, bem como a atividade dos sistemas proteolíticos lisossomal¸ ubiquitina-proteassoma e dependente de Ca+2. A superexpressão in vivo da Ucn2 por 14 dias promoveu hipertrofia e preveniu a atrofia em músculos tibialis anterior de camundongos normais e submetidos ao modelo de desnervação motora isquiática.Resumo Este crescimento muscular induzido pela Ucn2 in vivo foi associado a ativação das vias de sinalização AMPc/PKA/CREB, AMPc/Epac, Akt/mTOR/S6, Akt/mTOR/4E-BP1 e ERK1/2/eIF4E com consequente estimulação da síntese proteica. Em concordância, utilizando uma técnica de manipulação genética in vivo, demonstramos que a hipertrofia promovida pela Ucn2 é dependente da estimulação das cascatas de sinalização ativadas por Akt e ERK1/2. Ademais, essa alteração fenotípica promovida pela Ucn2 induziu melhora da resistência à fadiga muscular, sendo este impacto funcional dependentente de ERK1/2, mas não de Akt. Além disso, a superexpressão da Ucn2 induziu \"shifting\" para o tipo de fibra oxidativa (tipo I), sendo esta plasticidade possivelmente mediada por PGC-1?, o que pode ter contribuído pelo menos em parte, para o efeito benéfico promovido pela Ucn2 na função muscular. O efeito antiatrófico da Ucn2 in vivo foi associado à estimulação da via Akt/Foxo1,3 concomitante com a redução da atividade transcricional de Foxo, resultando na diminuição da expressão da E3-ligase atrogin-1 e do gene autofágico LC3. Em paralelo, a Ucn2 in vivo promoveu inibição do fluxo autofágico, inferido pelo acúmulo das proteínas LC3-I, LC3-II e p62 nestes músculos. Corroborando os achados in vivo, os efeitos antiproteolíticos da Ucn2 in vitro parecem ser mediados pelo AMPc e envolvem a supressão da atividade do sistema lisossomal/autofágico em músculos EDL de ratos normais. Portanto, além da participação de efetores dowsntream do AMPc, como PKA e EPAC, diferentes quinases participam dos efeitos biológicos da Ucn2 na musculatura esquelética. Esses resultados são importantes para caracterizar novas estratégias terapêuticas capazes de atuar no combate à atrofia muscular em diversas situações catabólicas.Urocortin 2 (Ucn2) is a peptide that belongs to corticotrophin releasing factors (CRF) family and, as well as its specific receptor CRF2R? (corticotropin releasing factor receptor type 2?), are expressed in skeletal muscle. Although it has been demonstrated that Ucn2 systemic treatment is able to induce hypertrophy and prevent loss of muscle mass, nothing is known about the molecular mechanisms through which Ucn2 plays its biological actions. The main objective of this work was to investigate the Ucn2 mechanism of action in rodent skeletal muscle for the appearance of the hypertrophic response and the possible participation of Akt/mTOR, Akt/Foxo and ERK1/2 signaling pathways in this anabolic effect. For this, an in vivo transfection model of Ucn2 was used by the electroporation method in tibialis anterior muscles of mice. Were quantified in these muscles: 1) the phosphorylation state of effector components of these pathways; 2) signaling molecules of the autophagic pathway; 3) the rate of protein synthesis in vivo and 4) the expression of genes related to muscle atrophy (atrogenes). Another methodology used to verify the direct effect of Ucn2 in skeletal muscle was the incubation of soleus and EDL muscles isolated from rodents with this peptide in vitro in order to investigate the total rate of protein degradation, as well as the activity of the lysosomal, ubiquitin-proteasome and Ca+2 dependent proteolytic systems. Ucn2 overexpression in vivo for 14 days promoted hypertrophy and prevented atrophy in tibialis anterior muscles of normal mice and submitted to the sciatic motor denervation model. This muscle growth induced by Ucn2 in vivo was associated with the activation ofAbstract cAMP/PKA/CREB, cAMP/Epac, Akt/mTOR/S6, Akt/mTOR/4E-BP1 and ERK1/2/eIF4E signaling pathways with consequent stimulation of protein synthesis. In agreement, using a genetic manipulation technique in vivo, we demonstrated that the hypertrophy promoted by Ucn2 is dependent on the stimulation of the signaling cascades activated by Akt and ERK1/2. In addition, this phenotypic alteration promoted by Ucn2 induced an improvement in muscle fatigue resistance, being this functional impact dependent on ERK1/2, but not on Akt. Moreover, Ucn2 overexpression in vivo induced the shift to type I oxidative fiber, and this plasticity is possibly mediated by PGC-1?, which may have contributed at least in part to the beneficial effect promoted by Ucn2 in muscle function. The anti-atrophic effect of Ucn2 in vivo was associated with the stimulation of Akt/Foxo1,3 pathway concomitant with the reduction of Foxo transcriptional activity, resulting in a decrease in the expression of the atrogin-1 E3-ligase and of the autophagic gene LC3. In parallel, Ucn2 in vivo promoted inhibition of autophagic flow, inferred by the accumulation of LC3-I, LC3-II and p62 proteins in these muscles. Corroborating the in vivo findings, the antiproteolytic effects of Ucn2 in vitro appear to be mediated by cAMP and involve the suppression of lysosomal/autophagic system activity in EDL muscles of normal rats. Thus, in addition to the participation of cAMP dowsntream effectors, such as PKA and EPAC, different kinases participate in the biological effects of Ucn2 on skeletal muscle. These results are important to characterize new therapeutic strategies able to prevent muscular atrophy in several catabolic situations.
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Oliveira, Leandro Augusto de. "Estudo do envolvimento da neurotransmissão CRFérgica do Núcleo Leito da Estria Terminal (NLET) nas respostas autonômicas desencadeadas pelo estresse por restrição agudo em ratos." Universidade Federal de São Carlos, 2015. https://repositorio.ufscar.br/handle/ufscar/7161.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
The corticotropin-releasing factor (CRF) is involved in behavioral and physiological responses to emotional stress through its action in several limbic structures, including the bed nucleus of the stria terminalis (BNST). Nevertheless, the role of CRF1 and CRF2 receptors in the BNST in autonomic adjustments during aversive threat is unknown. Therefore, in the present study we investigated the involvement of CRF receptors within the BNST in autonomic responses evoked by the acute restraint stress in rats. For this, we evaluated the effects of bilateral treatment of the BNST with selective agonists and antagonists of either CRF1 or CRF2 receptors in the arterial pressure and heart rate increase and the decrease in tail skin temperature induced by restraint stress. Microinjection of the selective CRF1 receptor antagonist CP376395 into the BNST reduced the pressor and tachycardiac responses caused by restraint. Conversely, BNST treatment with the selective CRF1 receptor agonist CRF increased restraint-evoked arterial pressure and HR responses and reduced the fall in tail skin temperature response. All effects of CRF were inhibited by local BNST pretreatment with CP376395. The selective CRF2 receptor antagonist antisauvagine-30 reduced the arterial pressure increase and the fall in tail skin temperature. The selective CRF2 receptor agonist urocortin-3 increased restraint-evoked pressor and tachycardiac responses and reduced the drop in cutaneous temperature. All effects of urocortin-3 were abolished by local BNST pretreatment with antisauvagine-30. These findings indicate an involvement of both CRF1 and CRF2 receptors in the BNST in autonomic adjustments during emotional stress.
O fator liberador de corticotropina (CRF) está envolvido em respostas comportamentais e fisiológicas ao estresse emocional por meio de sua ação em várias estruturas límbicas, incluindo o núcleo leito da estria terminal (NLET). No entanto, o papel dos receptores CRF1 e CRF2 no NLET nas respostas autonômicas durante situações aversivas é desconhecido. Portanto, no presente estudo nós investigamos o envolvimento de receptores de CRF do NLET nas respostas autonômicas evocadas pelo estresse de restrição agudo em ratos. Para isso, foram avaliados os efeitos do tratamento bilateral do NLET com agonistas e antagonistas seletivos dos receptores CRF1 ou CRF2 nas respostas de aumento da pressão arterial e frequência cardíaca e de diminuição da temperatura cutânea da cauda induzidas pelo estresse por restrição agudo. Microinjeção do antagonista seletivo do receptor CRF1, CP376395, no NLET reduziu as respostas de aumento da pressão arterial e frequência cardíaca evocadas pelo estresse por restrição. Por outro lado, o tratamento do NLET com o agonista seletivo do receptor CRF1, CRF, causou um aumento das respostas pressora e taquicárdica e reduziu a resposta de queda de temperatura cutânea da cauda. Os efeitos do CRF foram inibidos pelo pré-tratamento do NLET com CP376395. O antagonista seletivo do receptor CRF2, antisauvagine-30, reduziu o aumento da pressão arterial e a queda da temperatura cutânea da cauda induzidas pelo estresse por restrição. O agonista seletivo do receptor CRF2, urocortina-3, potenciou as respostas pressora e taquicárdica e reduziu a queda na temperatura cutânea da cauda. Todos os efeitos da urocortina-3 foram abolidos pelo pré-tratamento local no NLET com antisauvagine-30. Esses resultados indicam um envolvimento de ambos os receptores CRF1 e CRF2 no NLET nos ajustes autonômicos durante o estresse emocional.
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Martin, Andrew Michael. "Urocortin in the hypothalamo-neurohypophyseal system." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.768190.
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Combs, Charlotte Emma. "The role of urocortin in osteoclast physiology." Thesis, St George's, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517193.
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Souto, Suzana Souza. "Eferências do núcleo lateral superior da oliva no rato (rattus norvegicus)." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-20122007-162508/.
Full textAbstract:
Após a descrição da Urocortina 1, um neuropeptídeo encontrado principalmente no núcleo de Edinger-Westphal e no núcleo lateral superior da oliva (LSO), atentou-se para a ausência do conhecimento das projeções de ambos os núcleos. Nós pretendemos contribuir para o conhecimento das projeções ascendentes e descendentes do LSO, usando um traçador neuronal anterógrado. Nós utilizamos o Biotin-Dextran-Amine (BDA) injetado no LSO de ratos, 15 a 20 dias depois os ratos eram perfundidos, os encéfalos e medulas foram seccionados e tratados histoquimicamente. Nós encontramos que existem 4 vias eferentes do LSO, tanto ascendentes como descendentes no sistema nervoso central, como segue: duas vias ascendentes, uma ipsilateral à injeção, a mais proeminente e a via contralateral que é menos densa; duas vias descendentes, uma ipsilateral muito menos evidente, e a contralateral que é moderada. Seguindo a via ascendente ipsilateral, nós encontramos as seguintes estruturas bem marcadas com BDA: o próprio LSO, núcleo do corpo trapezóide, o lemnisco lateral e seus núcleos, colículos inferior e superior e os seguintes núcleos talâmicos: suprageniculado, geniculado medial, partes dorsal e medial e córtex somatosensorial primário. Seguindo a via descendente contralateral nós encontramos as seguintes estruturas: o LSO ipsi e contralateral, o núcleo do corpo trapezóide, núcleo coclear ventral, parte anterior, núcleo coclear dorsal, núcleo coclear ventral, parte posterior e VIII nervo. Os dados que nós encontramos neste trabalho sugerem que as vis do LSO podem se estender até o córtex somatosensorial no prosencéfalo e o complexo de núcleos cocleares no tronco, enviando colaterais para os principais núcleos relacionados a via auditiva, provavelmente contribuindo para a localização da fonte sonora, em acordo com a anatomia desta informação sensorial específica.After the discovery of the Urocortin-1, a neuropeptide found mainly in the Edinger-Westphal nucleus and in the lateral superior olive nucleus (LSO), the attention was caught about the lack of known projections of both nuclei. We intended to contribute to the knowledge of both ascending and descending projections of the LSO, using a neuronal anterograde tracer. In order to do that we use the Biotin-Dextran-Amine (BDA) injected in the LSO of rats, fifteen to twenty days later the rats were perfused, the brains and spinal cords were cut and the sections treated histochemically. We have found that there are four pathways leaving the LSO either ascending or descending in the central nervous system, as following: two ascending pathways, one ipsilateral to the injection, the most proeminent one and the contralateral pathway that is less dense; two descending pathways, one ipsilateral, much less evident, and the contralateral that is very moderate. Tracking the ipsilateral ascending pathway we have found the following structures well labeled with BDA: the LSO itself, nucleus of the trapezoid body, the lateral lemniscus and its nuclei, inferior and superior colliculus, the following thalamic nuclei: suprageniculate, medial geniculate, dorsal and medial parts and the primary somatosensory cortex. Tracking the contralateral descending pathway we have found the following structures: the LSO ipsi and contralateral; the nucleus of the trapezoid body; ventral cochlear nucleus, anterior part; dorsal cochlear nucleus; ventral cochlear nucleus, posterior part and, the eight nerve. The data we have found in this work suggests that the pathways from the LSO could reach as far as the somatosensory cortex in the prosencephalon and the cochlear complex nuclei in the brainstem, sending collaterals to the main nuclei related to the auditory pathway, probably contributing to the localization of the sound source, due to the anatomy of this specific sensory information.
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Silva, André Valerio da. "Estudo das projeções hipotalâmicas para a região urocortinérgica do complexo oculomotor." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-27092010-105116/.
Full textAbstract:
O neuropeptídeo urocortina 1 (UCN 1) tem entre os seus principais locais de expressão o núcleo de Edinger-Westphal (EW) e o núcleo lateral superior da oliva. Após sua descoberta, sugeriu-se que o EW e o núcleo paraventricular do hipotálamo (PVH) possuíssem papéis complementares e opostos na resposta ao estresse, porém, não existem trabalhos que relacionam anatomicamente núcleos hipotalâmicos e o EW. A fim de contribuir para esta área foi proposto o mapeamento das aferências hipotalâmicas do EW, através da injeção de Fluoro-Gold neste núcleo e posterior mapeamento de suas aferências. Os resultados encontrados foram: PVH, área hipotalâmica lateral (LHA) e o núcleo posterior do hipotálamo (PH) e outras regiões do sistema nervoso central. Para controle, o traçador anterógrado Amina Dextrana Biotinilada, foi injetado nos núcleos/áreas hipotalâmicas PVH, LHA e PH sendo encontradas fibras próximas as células urocortinérgicas do EW. Nossos dados mostram um possível envolvimento das células UCN 1 do EW com o controle de funções autonômicas e neuroendócrinas.The neuropeptide urocortin 1 (UCN 1) has its main sites of expression at the Edinger-Westphal nucleus (EW) and the lateral superior olivary nucleus. After its discovery has suggested that EW and paraventricular nucleus of hypothalamus (PVH) have complementary and opposing roles in the stress response. However, there are no works relating anatomically the hypothalamic nuclei and EW. To contribute to this area we proposed mapping the hypothalamic afferents of the EW. We have used the Fluoro-Gold injected in the EW as a result of we have found retrogradely labeled cells in the following nuclei: PVH, lateral hypothalamic area (LHA), posterior hypothalamic nucleus (PH) and other regions of the central nervous system. For control, the anterograde tracer biotinylated dextran amine was injected into the nuclei/areas hypothalamic PVH, LHA, and PH we have found anterogradely labeled fibers in a very close apposition over urocortinergic cells at EW. Based on these data we are suggesting a involvement of cells with UCN 1 EW control of autonomic and neuroendocrine functions.
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Ribeiro, Diana Raquel Santos. "The role of urocortin-2 in pulmonary arterial hypertension." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/15381.
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Mestrado em Biologia Molecular e CelularPulmonary arterial hypertension (PAH) is a syndrome based on diverse aetiologies, characterized by a persistent increase in pulmonary vascular resistance and overload of the right ventricle (RV), leading to heart failure (HF) and death. Urocortin (UCN)-2 is a peptide highly expressed in the cardiovascular system that has shown promising therapeutic effects in several studies both in humans and animal models of HF. Thus, this study aims to explore the effects of UCN-2 treatment in an animal model of RV HF secondary to PAH and its impact on myocardial function. Male Wistar rats (180-200g) randomly received monocrotaline (MCT, 60mg/kg) or vehicle. After 14 days, animals were randomly assigned to receive UCN-2 treatment (5μg/kg/day) or vehicle. The study resulted in 4 groups: CTRL (n=9), CTRL+UCN-2 (n=9), MCT (n=7) and MCT+UCN-2 (n=10). Echocardiographic, hemodynamic studies and sample collection were performed 24-25 days after MCT administration. Only significant results (mean±SEM, p<0.05) are given. MCT animals developed PAH, demonstrated by impaired pulmonary flow, RV dilation and increased RV pressures, as well as decreased cardiac output. MCT administration also resulted in RV hypertrophy. UCN-2 treatment was able to restore PAH-induced severe abnormalities in cardiac function and structure. Moreover, Kaplan-Meier analysis showed increased survival rate for MCT+UCN-2 rats when compared with the MCT group. The molecular studies revealed an altered genetic expression of the UCN-2/CRHR2 system components in the MCT animals, as shown by the increase in molecular markers of hypertrophy, overload, hypoxia and apoptosis that were reversed with UCN-2 treatment. As well as an impaired protein activation/phosphorylation seen in peptides pertaining to different signaling pathways. In conclusion, we show that UCN-2 chronic treatment is able to restore PAHinduced severe abnormalities in cardiac function and structure, as well as to reverse the changes in the expression of markers of cardiac overload, hypertrophy, hypoxia and apoptosis induced by the disease. The beneficial effects of UCN-2 seem to be associated with the modulation of numerous signaling pathways, such as survival and proliferation. These findings suggest that the UCN-2/CRHR2 pathway has a relevant role on the pathophysiology of PAH and progression to RV failure, representing a potential therapeutic target.
A hipertensão arterial pulmonar (HAP) é uma síndrome caracterizada por um aumento progressivo das resistências vasculares pulmonares e sobrecarga sobre o ventrículo direito que potencialmente levam à insuficiência cardíaca (IC) direita e consequentemente à morte. A urocortina (UCN)-2 é um péptido altamente expresso a nível cardiovascular que tem exibido efeitos terapêuticos benéficos tanto em humanos como em modelos animais de IC. Este estudo tem como principal objetivo explorar os efeitos da UCN-2 num modelo animal de IC ventricular direita (VD), secundário à HAP, e o seu impacto na função miocárdica. Ratos Wistar machos receberam aleatoriamente uma injeção de monocrotalina (MCT) ou veículo. Após 14 dias, os animais foram novamente sorteados para receber tratamento com UCN-2 ou veículo. Do estudo resultaram 4 grupos experimentais: CTRL, CTRL+UCN-2, MCT e MCT+UCN-2. As avaliações ecocardiográficas, estudos hemodinâmicos e colheita de amostras para análise morfométrica, histológica e molecular foram realizados 24-25 dias após a administração de MCT. Os animais injetados com MCT desenvolveram HAP e IC VD, demonstrado pelo comprometimento do fluxo pulmonar, dilatação VD e aumento das pressões VD, assim como um débito cardíaco diminuído. A administração de MCT também levou à hipertrofia VD. O tratamento com UCN-2 conseguiu recuperar as alterações induzidas pela HAP na função e estrutura cardíacas. Ainda, os animais MCT+UCN-2 tiveram uma maior taxa de sobrevivência quando comparados com os MCT. Os estudos moleculares revelaram uma expressão genética e uma fosforilação proteica alterada nos animais MCT, de alguns componentes do sistema UCN-2/CRHR2. Em suma, com este estudo demonstramos que o tratamento crónico com UCN-2 é capaz de restaurar as alterações induzidas pela HAP na função e estrutura cardíacas, assim como reverter as alterações na expressão de marcadores cardíacos de sobrecarga, hipertrofia, hipóxia e apoptose induzidos pela doença. Estes resultados sugerem que a via UCN-2/CRHR2 tem um papel relevante na fisiopatologia da HAP e progressão para IC, representando um potencial alvo terapêutico.
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Santilli, Giorgia. "Mechanisms of the protective effects of urocortin against cell death." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406706.
Full textBook chapters on the topic "Urocortine"
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Smani, Tarik. "Urocortin." In Encyclopedia of Signaling Molecules, 5846–48. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101942.
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Smani, Tarik. "Urocortin." In Encyclopedia of Signaling Molecules, 1–4. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101942-1.
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Parkes, David G., and Clive N. May. "Cardiac and Vascular Actions of Urocortin." In Hormones and the Heart in Health and Disease, 39–52. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-708-6_3.
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Wu, Vincent, Pu-Qing Yuan, Muriel Larauche, Lixin Wang, and Mulugeta Million. "Urocortins." In Handbook of Biologically Active Peptides, 1346–53. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-385095-9.00183-4.
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Richards, Mark, and Miriam Rademaker. "Urocortins." In Handbook of Biologically Active Peptides, 1428–36. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-385095-9.00194-9.
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Fekete, É. M., and E. P. Zorrilla. "Urocortins." In Encyclopedia of Stress, 804–11. Elsevier, 2007. http://dx.doi.org/10.1016/b978-012373947-6.00386-x.
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Amano, Masafumi. "Urocortins." In Handbook of Hormones, 28—e2C—1. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801028-0.00111-2.
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Amano, Masafumi. "Urocortins." In Handbook of Hormones, 49–52. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820649-2.00012-7.
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Furman, Brian L. "Urocortin." In xPharm: The Comprehensive Pharmacology Reference, 1–2. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.62835-1.
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Furman, B. L. "Urocortin☆." In Reference Module in Biomedical Sciences. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801238-3.96836-3.
Full textConference papers on the topic "Urocortine"
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Erchegyi, Judit, Jozsef Gulyas, Marilyn Perrin, Charleen Miller, Kathy Lewis, Wolfgang Fischer, Cindy Donaldson, and Jean Rivier. "Corticotropin Releasing Factor (CRF) and Urocortins (Ucns) Chimeras." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.044.
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Adão, Rui, Pedro Mendes-Ferreira, Diana Santos-Ribeiro, Carolina Maia-Rocha, Luís Pimentel, Cláudia Pinto, Eamon P. Mulvaney, et al. "Urocortin-2 improves right ventricular function and attenuates experimental pulmonary arterial hypertension." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3041.
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Adão, Rui, Simon C. Kraler, Senka Holzer, Adelino Leite-Moreira, Simon Sedej, and Carmen Brás-Silva. "Effects of urocortin-2 on cellular Ca2+ homeostasis in right heart failure induced by pulmonary artery hypertension." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa1634.
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