Ciliary neurotrophic factor promotes survival of neonatal rat islets via the BCL-2 anti-apoptotic pathway

dc.creatorRezende, LF
dc.creatorStoppiglia, LF
dc.creatorSouza, KLA
dc.creatorNegro, A
dc.creatorLangone, F
dc.creatorBoschero, AC
dc.date2007
dc.dateOCT
dc.date2014-11-15T16:41:51Z
dc.date2015-11-26T16:12:23Z
dc.date2014-11-15T16:41:51Z
dc.date2015-11-26T16:12:23Z
dc.date.accessioned2018-03-28T23:00:38Z
dc.date.available2018-03-28T23:00:38Z
dc.identifierJournal Of Endocrinology. Soc Endocrinology, v. 195, n. 1, n. 157, n. 165, 2007.
dc.identifier0022-0795
dc.identifierWOS:000250439200017
dc.identifier10.1677/JOE-07-0016
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/55926
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/55926
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/55926
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1267259
dc.descriptionCiliary neurotrophic factor (CNTF) belongs to the cytokine family and increases neuron differentiation and/or survival. Pancreatic islets are richly innervated and express receptors for nerve growth factors (NGFs) and may undergo neurotypic responses. CNTF is found in pancreatic islets and exerts paracrine effects in neighboring cells. The aim of this study was to investigate possible effects of CNTF on neonatal rat pancreatic islet differentiation and/or survival. For this purpose, we isolated pancreatic islets from neonatal rats (1-2 days old) by the collagenase method and cultured for 3 days in RPMI medium with (CNTF) or without (CTL) 1 nM CNTF. Thereafter, glucose-stimulated insulin secretion (RIA), general metabolism by (NAD(P)H production; MTS), glucose metabolism ((CO2)-C-14 production), gene (RT-PCR), protein expression (western blotting), caspase-3 activity (Asp-Glu-Val-Asp (DEVD)), and apoptosis (DNA fragmentation) were analyzed. Our results showed that CNTF-treated islets demonstrated reduced glucose-induced insulin secretion. CNTF treatment did not affect glucose metabolism, as well as the expression of mRNAs and proteins that are crucial for the secretory process. Conversely, CNTF significantly increased mRNA and protein levels related to cell survival, such as Cx36, PAX4, and BCL-2, reduced caspase-3 activity, and islet cells apoptosis, suggesting that CNTF does not affect islet cell differentiation and, instead, acts as a survival factor reducing apoptosis by increasing the expression of the antiapoptotic BCL-2 protein and decreasing caspase-3 activity.
dc.description195
dc.description1
dc.description157
dc.description165
dc.languageen
dc.publisherSoc Endocrinology
dc.publisherBristol
dc.publisherInglaterra
dc.relationJournal Of Endocrinology
dc.relationJ. Endocrinol.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectStimulated Insulin-secretion
dc.subjectNonobese Diabetic Mice
dc.subjectProgrammed Cell-death
dc.subjectPancreatic-islets
dc.subjectProtease Activity
dc.subjectGene-expression
dc.subjectFamily Proteins
dc.subjectBeta-cells
dc.subjectPkc-alpha
dc.subjectGlucose
dc.titleCiliary neurotrophic factor promotes survival of neonatal rat islets via the BCL-2 anti-apoptotic pathway
dc.typeArtículos de revistas


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