Document Detail


c-Jun is regulated by combination of enhanced expression and phosphorylation in acute-overloaded rat heart.
MedLine Citation:
PMID:  14512277     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The transient increase in the expression of transcription factors encoded by immediate-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 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 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 activator protein-1 (AP-1) complex was observed after 10 and 30 min of pressure overload and Supershift assays confirmed that c-Jun was a major component of activated AP-1 complex. Moreover, experiments performed with the specific JNK inhibitor SP-600125 abolished c-Jun phosphorylation and markedly attenuated its expression as well as the expression of the fetal gene beta-myosin heavy chain. 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.
Authors:
Wilson Nadruz; Claudia B Kobarg; Jörg Kobarg; Kleber G Franchini
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2003-09-25
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  286     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2004 Feb 
Date Detail:
Created Date:  2004-01-12     Completed Date:  2004-03-09     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H760-7     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, School of Medicine, State University of Campinas, São Paulo, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anthracenes / pharmacology
Base Sequence
Cell Nucleus / physiology
Cytosol / physiology
Enzyme Activation
Enzyme Inhibitors / pharmacology
Heart / drug effects,  physiology*,  physiopathology
Male
Mitogen-Activated Protein Kinase 8
Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism*
Models, Animal
Myosin Heavy Chains / drug effects,  genetics
Oligodeoxyribonucleotides
Phosphorylation
Pressure
Proto-Oncogene Proteins c-jun / antagonists & inhibitors,  genetics,  metabolism*
Rats
Rats, Wistar
Ventricular Function, Left / physiology
Chemical
Reg. No./Substance:
0/Anthracenes; 0/Enzyme Inhibitors; 0/Myosin Heavy Chains; 0/Oligodeoxyribonucleotides; 0/Proto-Oncogene Proteins c-jun; 0/anthra(1,9-cd)pyrazol-6(2H)-one; EC 2.7.11.24/Mitogen-Activated Protein Kinase 8; EC 2.7.11.24/Mitogen-Activated Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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