期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 376, 期 4, 页码 677-681出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.09.057
关键词
AMPK; Cardiac hypertrophy; p70S6K; Heart; Isoproterenol
资金
- Fonds National de la Recherche Scientifique et Medicale, Belgium [3.4568.05]
- European Commission [QLG1-CT-2001-01488, LSHM-CT-2004-005272]
- Institut National de la Sante et de la Recherche Medicale, France
- Fondation de France
- Fonds Speciaux de Recherche
- Universite catholique de Louvain, Belgium
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.
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