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The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease
Published on: October 3, 2012
Parkin affects mitochondrial function and apoptosis in neuronal and myogenic cells
Yukiko Kuroda1, Takao Mitsui, Makoto Kunishige
1Department of Medicine and Bioregulatory Sciences, University of Tokushima Graduate School of Medicine, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Abstract:
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-1 cells. Expressions and enzymatic activities of mitochondrial respiratory chain complexes were not uniformly enhanced but those of complex 1 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.
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