Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348594
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampSouza, Kleber Luiz de Araujo e-
dc.contributor.authorunicampCarneiro, Everardo Magalhães-
dc.contributor.authorunicampBoschero, Antonio Carlos-
dc.typeArtigopt_BR
dc.titlePancreatic islets from dexamethasone-treated rats show alterations in global gene expression and mitochondrial pathwayspt_BR
dc.contributor.authorRoma, Leticia P.-
dc.contributor.authorSouza, Kleber L. A.-
dc.contributor.authorCarneiro, Everardo M.-
dc.contributor.authorBoschero, Antonio C.-
dc.contributor.authorBosqueiro, Jose R.-
dc.subjectExpressão gênicapt_BR
dc.subject.otherlanguageGene expressionpt_BR
dc.description.abstractChronic administration of glucocorticoids (GC) leads to characteristic features of type 2 diabetes in mammals. The main action of dexamethasone in target cells occurs through modulation of gene expression, although the exact mechanisms are still unknown. We therefore investigated the gene expression profile of pancreatic islets from rats treated with dexamethasone using a cDNA array screening analysis. The expression of selected genes and proteins involved in mitochondria] apoptosis was further analyzed by PCR and immunoblotting. Insulin, triglyceride and free fatty acid plasma levels, as well as glucose-induced insulin secretion, were significantly higher in dexamethasone-treated rats compared with controls. Out of 1176 genes, 60 were up-regulated and 28 were down-regulated by dexamethasone treatment. Some of the modulated genes are involved in apoptosis, stress response, and proliferation pathways. RT-PCR confirmed the cDNA array results for 6 selected genes. Bax alpha protein expression was increased, while Bcl-2 was decreased. In vivo dexamethasone treatment decreased the mitochondrial production of NAD(P)H, and increased ROS production. Concluding, our data indicate that dexamethasone modulates the expression of genes and proteins involved in several pathways of pancreatic-islet cells, and mitochondria dysfunction might be involved in the deleterious effects after long-term GC treatmentpt_BR
dc.relation.ispartofGeneral physiology and biophysicspt_BR
dc.relation.ispartofabbreviationGen physiol biophyspt_BR
dc.publisher.cityBratislavapt_BR
dc.publisher.countryEslováquiapt_BR
dc.publisherAEPresspt_BR
dc.date.issued2012-
dc.date.monthofcirculationMar.pt_BR
dc.language.isoengpt_BR
dc.description.volume31pt_BR
dc.description.issuenumber1pt_BR
dc.description.firstpage65pt_BR
dc.description.lastpage76pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0231-5882pt_BR
dc.identifier.eissn1338-4325pt_BR
dc.identifier.doi10.4149/gpb_2012_011pt_BR
dc.identifier.urlhttp://www.elis.sk/index.php?page=shop.product_details&flypage=flypage.tpl&product_id=2724&category_id=94&option=com_virtuemart&vmcchk=1&Itemid=1pt_BR
dc.description.sponsorshipCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQpt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.description.sponsordocumentnumber04/14494-6pt_BR
dc.date.available2020-09-02T20:35:59Z-
dc.date.accessioned2020-09-02T20:35:59Z-
dc.description.provenanceSubmitted by Sanches Olivia (olivias@unicamp.br) on 2020-09-02T20:35:59Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:12:26Z : No. of bitstreams: 1 000301816200008.pdf: 458078 bytes, checksum: b339d78e37bdea28df06d1b57adf3ce1 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-02T20:35:59Z (GMT). No. of bitstreams: 0 Previous issue date: 2012en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348594-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.departmentDepartamento de Biologia Estrutural e Funcionalpt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.subject.keywordCell viabilitypt_BR
dc.subject.keywordInsulin secretionpt_BR
dc.subject.keywordDiabetespt_BR
dc.identifier.source000301816200008pt_BR
dc.creator.orcid0000-0003-3537-2456pt_BR
dc.creator.orcid0000-0003-3212-369Xpt_BR
dc.creator.orcid0000-0003-3829-8570pt_BR
dc.type.formArtigopt_BR
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