Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/1795
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleThe Regulation of Rasd1 Expression by Glucocorticoids and Prolactin Controls Peripartum Maternal Insulin Secretionpt_BR
dc.contributor.authorLellis-Santos, Camilopt_BR
dc.contributor.authorSakamoto, Luciano H.pt_BR
dc.contributor.authorBromati, Carla R.pt_BR
dc.contributor.authorNogueira, Tatiane C. A.pt_BR
dc.contributor.authorLeite, Adriana R.pt_BR
dc.contributor.authorYamanaka, Tatiana S.pt_BR
dc.contributor.authorKinote, Andrezzapt_BR
dc.contributor.authorAnhe, Gabriel F.pt_BR
dc.contributor.authorBordin, Silvanapt_BR
unicamp.authorKinote, Andrezzapt_BR
unicamp.authorAnhe, Gabriel F.pt_BR
unicamp.author.externalLellis-Santos, Camilopt
unicamp.author.externalSakamoto, Luciano H.pt
unicamp.author.externalBromati, Carla R.pt
unicamp.author.externalNogueira, Tatiane C. A.pt
unicamp.author.externalLeite, Adriana R.pt
unicamp.author.externalYamanaka, Tatiana S.pt
unicamp.author.externalBordin, Silvanapt
dc.subject.wos11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1pt_BR
dc.subject.wosOBESE ZUCKER RATSpt_BR
dc.subject.wosBETA-CELL MASSpt_BR
dc.subject.wosGENE-EXPRESSIONpt_BR
dc.subject.wosLACTOGENIC HORMONESpt_BR
dc.subject.wosSIGNAL TRANSDUCERpt_BR
dc.subject.wosPANCREATIC-ISLETSpt_BR
dc.subject.wosDEXAMETHASONEpt_BR
dc.subject.wosDEXRAS1pt_BR
dc.subject.wosPROTEINpt_BR
dc.description.abstractThe transition from gestation to lactation is characterized by a robust adaptation of maternal pancreatic beta-cells. Consistent with the loss of beta-cell mass, glucose-induced insulin secretion is down-regulated in the islets of early lactating dams. Extensive experimental evidence has demonstrated that the surge of prolactin is responsible for the morphofunctional remodeling of the maternal endocrine pancreas during pregnancy, but the precise molecular mechanisms by which this phenotype is rapidly reversed after delivery are not completely understood. This study investigated whether glucocorticoid-regulated expression of Rasd1/Dexras, a small inhibitoryGprotein, is involved in this physiological plasticity. Immunofluorescent staining demonstrated that Rasd1 is localized within pancreatic beta-cells. Rasd1 expression in insulin-secreting cells was increased by dexamethasone and decreased by prolactin. In vivo data confirmed that Rasd1 expression is decreased in islets from pregnant rats and increased in islets from lactating mothers. Knockdown of Rasd1 abolished the inhibitory effects of dexamethasone on insulin secretion and the protein kinase A, protein kinase C, and ERK1/2 pathways. Chromatin immunoprecipitation experiments revealed that glucocorticoid receptor (GR) and signal transducer and activator of transcription 5b (STAT5b) cooperatively mediate glucocorticoid-induced Rasd1 expression in islets. Prolactin inhibited the stimulatory effect of GR/STAT5b complex on Rasd1 transcription. Overall, our data indicate that the stimulation of Rasd1 expression by glucocorticoid at the end of pregnancy reverses the increased insulin secretion that occurs during pregnancy. Prolactin negatively regulates this pathway by inhibiting GR/STAT5b transcriptional activity on the Rasd1 gene. (Endocrinology 153: 3668-3678, 2012)pt
dc.relation.ispartofEndocrinologypt_BR
dc.publisher.cityChevy Chasept_BR
dc.publisherEndocrine Socpt_BR
dc.date.issued2012pt_BR
dc.identifier.citationEndocrinology. Endocrine Soc, v.153, n.8, p.3668-3678, 2012pt_BR
dc.language.isoengpt_BR
dc.description.volume153pt_BR
dc.description.issuenumber8pt_BR
dc.description.firstpage3668pt_BR
dc.description.lastpage3678pt_BR
dc.rightsfechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0013-7227pt_BR
dc.identifier.wosidWOS:000306652400015pt_BR
dc.identifier.doi10.1210/en.2012-1135pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorship1Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorship1Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.date.available2013-09-19T18:05:52Z
dc.date.available2016-07-01T15:17:33Z-
dc.date.accessioned2013-09-19T18:05:52Z
dc.date.accessioned2016-07-01T15:17:33Z-
dc.description.provenanceMade available in DSpace on 2013-09-19T18:05:52Z (GMT). No. of bitstreams: 0 Previous issue date: 2012en
dc.description.provenanceMade available in DSpace on 2016-07-01T15:17:33Z (GMT). No. of bitstreams: 0 Previous issue date: 2012en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/1795
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/1795-
dc.contributor.departmentFarmacologia
dc.contributor.unidadeFCMpt
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