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1 Department of Internal Medicine, State University of Campinas, Campinas, SP, Brazil
* To whom correspondence should be addressed. E-mail: franchin{at}obelix.unicamp.br.
The transient increase in the expression of transcription factors encoded by immediately early genes has been considered to play a critical role in the coordination of early gene expression during the hypertrophic growth of cardiac myocytes. Here we investigated the regulation of c-Jun and its upstream activators c-Jun N-terminal Kinases (JNKs) in the myocardium of rats subjected to acute pressure overload induced by transverse aortic constriction. Western blotting and immunohistochemistry analysis demonstrated that both JNK1 and JNK2 were transiently activated by pressure overload, but only JNK1 was found to be activated at the nuclei of cardiac myocytes. JNK1 activation was paralleled by phosphorylation of c-Jun at serine-63 in the myocardial nuclear fraction and by an increase in c-Jun expression in cardiac myocytes. A consistent increase in DNA-binding of AP1 complex was observed after 10 and 30 minutes of pressure overload and Supershift assays confirmed that c-Jun was a major component of activated AP1 complex. Moreover, experiments performed with the specific JNK inhibitor SP600125 abolished c-Jun phosphorylation and markedly attenuated its expression as well as the expression of the fetal gene 
-myosin heavy chain (-MHC). Overall, these findings demonstrate a molecular basis for load-induced activation of c-Jun in cardiac myocytes and its connection with the regulation of fetal gene, characteristic of the acute response to pressure overload.
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