Leptin inhibits apoptosis in thymus through a Janus kinase-2-independent, insulin receptor substrate-1/phosphatidylinositol-3 kinase-dependent pathway

dc.creatorMansour, E
dc.creatorPereira, FG
dc.creatorAraujo, EP
dc.creatorAmaral, MEC
dc.creatorMorari, J
dc.creatorFerraroni, NR
dc.creatorFerreira, DS
dc.creatorLorand-Metze, I
dc.creatorVelloso, LA
dc.date2006
dc.dateNOV
dc.date2014-11-17T17:44:01Z
dc.date2015-11-26T16:45:23Z
dc.date2014-11-17T17:44:01Z
dc.date2015-11-26T16:45:23Z
dc.date.accessioned2018-03-28T23:30:58Z
dc.date.available2018-03-28T23:30:58Z
dc.identifierEndocrinology. Endocrine Soc, v. 147, n. 11, n. 5470, n. 5479, 2006.
dc.identifier0013-7227
dc.identifierWOS:000241324900053
dc.identifier10.1210/en.2006-0223
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80856
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/80856
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/80856
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1274200
dc.descriptionThe cytokine-like hormone leptin is known to exert important functions on the modulation of immune responses. Some of these effects are dependent on the property of leptin to modulate the apoptosis of thymic cells. In the present study, we used Wistar rats to investigate the molecular mechanisms involved in leptin-dependent control of apoptosis in thymus. Apoptosis was evaluated by flow cytometry and ELISA for nucleosome determination, whereas signal transduction was evaluated by immunoprecipitation, immunoblot, and confocal microscopy. The Ob receptor (ObR) was expressed in most thymic cells and its relative amount reduced progressively during thymocyte maturation. ObR expression was colocalized with Janus kinase (JAK)-2 and signal transducer and activator of transcription-3, and an acute, in vivo, injection of leptin promoted the tyrosine phosphorylation of JAK-2 and the engagement of signal transducer and activator of transcription-3. The treatment with leptin also led to the tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and serine phosphorylation of Akt. Chronic treatment with leptin reduced thymic apoptosis, an effect that was not inhibited by the JAK inhibitor AG490 but was significantly inhibited by the phosphatidylinositol 3-kinase inhibitor LY294002 and an antisense oligonucleotide to IRS-1. Thus, leptin inhibits the apoptosis of thymic cells through a mechanism that is independent of the activation of JAK-2 but depends on the engagement of the IRS-1/phosphatidylinositol 3-kinase pathway.
dc.descriptiono TEXTO COMPLETO DESTE ARTIGO, ESTARÁ DISPONÍVEL À PARTIR DE AGOSTO DE 2015.
dc.description147
dc.description11
dc.description5470
dc.description5479
dc.languageen
dc.publisherEndocrine Soc
dc.publisherChevy Chase
dc.publisherEUA
dc.relationEndocrinology
dc.relationEndocrinology
dc.rightsembargo
dc.sourceWeb of Science
dc.subjectAkt Phosphorylation
dc.subjectSignaling Pathways
dc.subjectPancreatic-islets
dc.subjectImmune-response
dc.subjectT-lymphocytes
dc.subjectActivation
dc.subjectExpression
dc.subjectRat
dc.subjectMice
dc.subjectImmunodeficiency
dc.titleLeptin inhibits apoptosis in thymus through a Janus kinase-2-independent, insulin receptor substrate-1/phosphatidylinositol-3 kinase-dependent pathway
dc.typeArtículos de revistas


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