Acetylation-dependent regulation of mitochondrial ALDH2 activation by SIRT3 mediates acute ethanol-induced eNOS activation

Acetylation-dependent regulation of mitochondrial ALDH2 activation by SIRT3 mediates acute ethanol-induced eNOS activation

Moderate alcohol consumption has beneficial effects on endothelial nitric-oxide synthase (eNOS) activation, which can engender an array of anti-atherogenic actions. Here we show that in human aortic endothelial cells (HAECs), rapid activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) mediates ethanol-induced eNOS activation by preventing reactive oxygen species (ROS) accumulation. Furthermore, activation of ALDH2 by ethanol is due to its hyperacetylation by SIRT3 inactivation. These data suggest that ethanol-induced eNOS activation in HAECs may be dependent on ALDH2 hyperacetylation by SIRT3 inactivation. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

适度饮酒对内皮型一氧化氮合酶（eNOS）的激活具有有益作用，这可产生一系列抗动脉粥样硬化的作用。在此我们表明，在人主动脉内皮细胞（HAECs）中，线粒体乙醛脱氢酶2（ALDH2）的快速激活通过防止活性氧物质（ROS）的积累来介导乙醇诱导的eNOS激活。此外，乙醇对ALDH2的激活是由于SIRT3失活导致其过度乙酰化。这些数据表明，在HAECs中乙醇诱导的eNOS激活可能依赖于SIRT3失活引起的ALDH2过度乙酰化。（C）2011欧洲生物化学学会联合会。由爱思唯尔出版集团出版。保留所有权利。