Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/2291
Type: Artigo de periódico
Title: Pancreatic islets from dexamethasone-treated rats show alterations in global gene expression and mitochondrial pathways
Author: Roma, Leticia P.
Souza, Kleber L. A.
Carneiro, Everardo M.
Boschero, Antonio C.
Bosqueiro, Jose R.
Abstract: Chronic 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 treatment.
Subject: Gene expression
Cell viability
Insulin secretion
Diabetes
Editor: General Physiol And Biophysics
Rights: fechado
Identifier DOI: 10.4149/gpb_2012_011
Date Issue: 2012
Appears in Collections:IB - Artigos e Outros Documentos

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