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Acetylation‐dependent regulation of mitochondrial ALDH2 activation by SIRT3 mediates acute ethanol‐induced eNOS activation
Author(s) -
Xue Li,
Xu Feng,
Meng Lujing,
Wei Shujian,
Wang Jiali,
Hao Panpan,
Bian Yuan,
Zhang Yun,
Chen Yuguo
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.11.031
Subject(s) - sirt3 , enos , aldh2 , chemistry , ethanol , aldehyde dehydrogenase , reactive oxygen species , microbiology and biotechnology , mitochondrion , disulfiram , nitric oxide , biochemistry , nitric oxide synthase , sirtuin , nad+ kinase , biology , enzyme , organic chemistry
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.