Load-induced Transcriptional Activation Of C-jun In Rat Myocardium: Regulation By Myocyte Enhancer Factor 2

dc.creatorNadruz Jr W.
dc.creatorKobarg C.B.
dc.creatorConstancio S.S.
dc.creatorCorat P.D.C.
dc.creatorFranchini K.G.
dc.date2003
dc.date2015-06-30T17:28:18Z
dc.date2015-11-26T15:00:00Z
dc.date2015-06-30T17:28:18Z
dc.date2015-11-26T15:00:00Z
dc.date.accessioned2018-03-28T22:11:26Z
dc.date.available2018-03-28T22:11:26Z
dc.identifier
dc.identifierCirculation Research. , v. 92, n. 2, p. 243 - 251, 2003.
dc.identifier97330
dc.identifier10.1161/01.RES.0000053184.94618.97
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-0037423551&partnerID=40&md5=bf0625fd24808e559534b1da3b0ef781
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/102146
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/102146
dc.identifier2-s2.0-0037423551
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1256132
dc.descriptionThe increased expression of immediate-early genes is a key feature of the myocardial response to hypertrophic stimuli. In this study, we investigated whether pressure overload or phenylephrine treatment stimulated myocyte enhancer factor 2 (MEF2)-dependent transcriptional activation of c-jun in cardiac myocytes. Western blotting and immunohistochemical analysis of rat myocardium demonstrated that p70MEF2 is highly expressed in the rat heart and is predominantly located at the nuclei of cardiac myocytes. Electrophoretic mobility shift assays of myocardial nuclear extracts revealed a consistent DNA binding activation of MEF2 after 1 and 2 hours of pressure overload. We further showed that pressure overload induced a progressive nuclear translocation and activation of extracellular signalregulated kinase 5 (ERK5). Coimmunoprecipitation and in vitro kinase assays indicated that the activation of ERK5 was paralleled by increased association of ERK5/p70MEF2 and by enhanced ability of ERK5 to phosphorylate p70MEF2. Experiments with in vivo transfection of the left ventricle with the c-jun promoter reporter gene showed that pressure overload induced a consistent increase of c-jun transcriptional activity in the rat myocardium. Rendering the MEF2 site of the c-jun plasmid inactive by mutation abolished the load-induced activation of the c-jun promoter reporter gene. Mutation of the MEF2 site also abolished the phenylephrine-induced c-jun promoter activation in neonatal rat ventricular myocytes. In addition, we demonstrated that neonatal rat ventricular myocyte transfection with ERK5antisense oligodeoxynucleotide inhibited the phenylephrine-induced c-jun promoter activation. These findings identify MEF2 as a potential regulator of c-jun transactivation and suggest that ERK5 might be an important mediator of MEF2 and c-jun promoter activation in response to hypertrophic stimuli in cardiac myocytes.
dc.description92
dc.description2
dc.description243
dc.description251
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dc.languageen
dc.publisher
dc.relationCirculation Research
dc.rightsfechado
dc.sourceScopus
dc.titleLoad-induced Transcriptional Activation Of C-jun In Rat Myocardium: Regulation By Myocyte Enhancer Factor 2
dc.typeArtículos de revistas


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