甲硫氨酸亚砜还原酶A保护神经元细胞免受短暂缺氧/复氧损伤。
Methionine sulfoxide reductase A protects neuronal cells against brief hypoxia/reoxygenation.
作者信息
Yermolaieva Olena, Xu Rong, Schinstock Carrie, Brot Nathan, Weissbach Herbert, Heinemann Stefan H, Hoshi Toshinori
机构信息
Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
出版信息
Proc Natl Acad Sci U S A. 2004 Feb 3;101(5):1159-64. doi: 10.1073/pnas.0308215100. Epub 2004 Jan 26.
Abstract
Hypoxia/reoxygenation induces cellular injury by promoting oxidative stress. Reversible oxidation of methionine in proteins involving the enzyme peptide methionine sulfoxide reductase type A (MSRA) is postulated to serve a general antioxidant role. Therefore, we examined whether overexpression of MSRA protected cells from hypoxia/reoxygenation injury. Brief hypoxia increased the intracellular reactive oxygen species (ROS) level in PC12 cells and promoted apoptotic cell death. Adenovirus-mediated overexpression of MSRA significantly diminished the hypoxia-induced increase in ROS and facilitated cell survival. Measurements of the membrane potentials of intact mitochondria in PC12 cells and of isolated rat liver mitochondria showed that hypoxia induced depolarization of the mitochondrial membrane. The results demonstrate that MSRA plays a protective role against hypoxia/reoxygenation-induced cell injury and suggest the therapeutic potential of MSRA in ischemic heart and brain disease.
摘要
缺氧/复氧通过促进氧化应激诱导细胞损伤。涉及A 型肽甲硫氨酸亚砜还原酶（MSRA）的蛋白质中甲硫氨酸的可逆氧化被认为具有一般抗氧化作用。因此，我们研究了MSRA的过表达是否能保护细胞免受缺氧/复氧损伤。短暂缺氧会增加PC12细胞内活性氧（ROS）水平并促进凋亡性细胞死亡。腺病毒介导的MSRA过表达显著减少了缺氧诱导的ROS增加并促进了细胞存活。对PC12细胞中完整线粒体以及分离的大鼠肝线粒体膜电位的测量表明，缺氧会诱导线粒体膜去极化。结果表明，MSRA对缺氧/复氧诱导的细胞损伤起保护作用，并提示MSRA在缺血性心脏和脑部疾病中的治疗潜力。
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