AMPKα2 counteracts the development of cardiac hypertrophy induced by isoproterenol

被引:56
|
作者
Zarrinpashneh, Elharn [1 ]
Beauloye, Christophe [1 ]
Ginion, Audrey [1 ]
Pouleur, Anne-Catherine [1 ]
Havaux, Xavier [1 ]
Hue, Louis [2 ]
Viollet, Benoit [3 ,4 ]
Vanoverschelde, Jean-Louis [1 ]
Bertrand, Luc [1 ]
机构
[1] Catholic Univ Louvain, Div Cardiol, B-1200 Brussels, Belgium
[2] Catholic Univ Louvain, de Duve Inst, Hormone & Metab Res Unit, B-1200 Brussels, Belgium
[3] Univ Paris 05, Inst Cochin, CNRS, UMR 8104, Paris, France
[4] INSERM, U567, Paris, France
关键词
AMPK; Cardiac hypertrophy; p70S6K; Heart; Isoproterenol;
D O I
10.1016/j.bbrc.2008.09.057
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 AMPK alpha 2 in the control of cardiac hypertrophy by using AMPK alpha 2-/- mice submitted to isoproterenol. The isoproterenol-induced cardiac hypertrophy, measured by left ventricular mass and histological examination, was significantly higher in AMPK alpha 2-/- than in WT animals. Moreover, the intensification of cardiac hypertrophy found in AMPK alpha 2-/- 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 AMPK alpha 2 plays a role of brake for the development of cardiac hypertrophy. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:677 / 681
页数:5
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