α-突触核蛋白与线粒体的关联会导致氧化应激。
Mitochondrial association of alpha-synuclein causes oxidative stress.
作者信息
Parihar M S, Parihar A, Fujita M, Hashimoto M, Ghafourifar P
机构信息
Department of Surgery, Davis Heart and Lung Research Institute, Ohio State University, 460 West 12th Avenue, Columbus, 43210 OH, USA.
出版信息
Cell Mol Life Sci. 2008 Apr;65(7-8):1272-84. doi: 10.1007/s00018-008-7589-1.
Alpha-synuclein is a neuron-specific protein that contributes to the pathology of Parkinson's disease via mitochondria-related mechanisms. The present study investigated possible interaction of alpha-synuclein with mitochondria and consequences of such interaction. Using SHSY cells overexpressing alpha-synuclein A53T mutant or wild-type, as well as isolated rat brain mitochondria, the present study shows that alpha-synuclein localizes at the mitochondrial membrane. In both SHSY cells and isolated mitochondria, interaction of alpha-synuclein with mitochondria causes release of cytochrome c, increase of mitochondrial calcium and nitric oxide, and oxidative modification of mitochondrial components. These findings suggest a pivotal role for mitochondria in oxidative stress and apoptosis induced by alpha-synuclein.
α-突触核蛋白是一种神经元特异性蛋白，通过与线粒体相关的机制参与帕金森病的病理过程。本研究调查了α-突触核蛋白与线粒体之间可能的相互作用以及这种相互作用的后果。使用过表达α-突触核蛋白A53T突变体或野生型的SHSY细胞以及分离的大鼠脑线粒体，本研究表明α-突触核蛋白定位于线粒体膜。在SHSY细胞和分离的线粒体中，α-突触核蛋白与线粒体的相互作用都会导致细胞色素c释放、线粒体钙和一氧化氮增加以及线粒体成分的氧化修饰。这些发现表明线粒体在α-突触核蛋白诱导的氧化应激和细胞凋亡中起关键作用。
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