Parkin affects mitochondrial function and apoptosis in neuronal and myogenic cells

被引：40

作者：

Kuroda, Yukiko ^{[1
]}

Mitsui, Takao ^{[1
]}

Kunishige, Makoto ^{[1
]}

Matsumoto, Toshio ^{[1
]}

机构：

[1] Univ Tokushima, Grad Sch Med, Dept Med & Bioregulatory Sci, Tokushima 7708503, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 348卷 / 03期

关键词：

respiratory chain complex; membrane potential; cytofluorometric analysis; siRNA;

D O I：

10.1016/j.bbrc.2006.06.201

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We investigated the effect of parkin on mitochondrial function and apoptosis in SH-SY5Y, L6, RD, and COS-1 cells. Wild-type parkin attenuated reactive oxygen species (ROS) production in SH-SY5Y cells and mutant parkin enhanced ROS production in SH-SY5Y and L6 cells. Reactive oxygen intermediates, that were detected in mitochondria, were decreased in cells with overexpression of parkin. Parkin prevented apoptosis and enhanced mitochondrial membrane potentials in SH-SY5Y and L6 cells not in COS-I cells. Expressions and enzymatic activities of mitochondrial respiratory chain complexes were not uniformly enhanced but those of complex I were selectively enhanced. The present results suggest the cell-selective function of parkin, i.e., parkin possesses anti-apoptotic and anti-oxidant function in neuronal or myogenic cells but not in kidney cells. (c) 2006 Elsevier Inc. All rights reserved.

引用

页码：787 / 793

页数：7

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