| Literature DB >> 18812163 |
Elham Zarrinpashneh1, Christophe Beauloye, Audrey Ginion, Anne-Catherine Pouleur, Xavier Havaux, Louis Hue, Benoit Viollet, Jean-Louis Vanoverschelde, Luc Bertrand.
Abstract
As AMP-activated protein kinase (AMPK) controls protein translation, an anti-hypertrophic effect of AMPK has been suggested. However, there is no genetic evidence to confirm this hypothesis. We investigated the contribution of AMPKalpha2 in the control of cardiac hypertrophy by using AMPKalpha2-/- mice submitted to isoproterenol. The isoproterenol-induced cardiac hypertrophy, measured by left ventricular mass and histological examination, was significantly higher in AMPKalpha2-/- than in WT animals. Moreover, the intensification of cardiac hypertrophy found in AMPKalpha2-/- mice can be linked to the abnormal basal overstimulation of the p70 ribosomal S6 protein kinase, an enzyme known to regulate protein translation and cell growth. In conclusion, this work shows that AMPKalpha2 plays a role of brake for the development of cardiac hypertrophy.Entities:
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Year: 2008 PMID: 18812163 DOI: 10.1016/j.bbrc.2008.09.057
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575