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

      Febs Letters
      Acetylation, drug effects, Acetyltransferases, genetics, metabolism, Aldehyde Dehydrogenase, Cells, Cultured, Dose-Response Relationship, Drug, Endothelial Cells, Enzyme Activation, Ethanol, pharmacology, Gene Expression Regulation, Enzymologic, Humans, Mitochondria, enzymology, Nitric Oxide Synthase Type III, Protein Processing, Post-Translational, RNA, Small Interfering, Reactive Oxygen Species, Sirtuin 3, Transfection

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          Abstract

          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. Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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