期刊
MOLECULAR NEUROBIOLOGY
卷 54, 期 8, 页码 6235-6244出版社
HUMANA PRESS INC
DOI: 10.1007/s12035-016-0104-z
关键词
Low-intensity ultrasound ( LIUS); 1-Methyl-4-phenylpyridiniumion ( MPP plus ); Parkinson's disease (PD); Mitochondrial dysfunction; alpha-Synuclein; Reactive oxygen species (ROS)
资金
- Inha University Research Grant
Many studies have shown that mitochondrial dysfunction and the subsequent oxidative stress caused by excessive reactive oxygen species (ROS) generation play a central role in the pathogenesis of Parkinson's disease (PD). We have previously shown that low-intensity ultrasound (LIUS) could reduce ROS generation by L-buthionine-(S, R)-sulfoximine (BSO) in retinal pigment epithelial cells. In this study, we studied the effects of LIUS stimulation on the ROS-dependent alpha-synuclein aggregation in 1-methyl-4-phenylpyridinium ion (MPP+)treated PC12 cells. We found that LIUS stimulation suppressed the MPP+-induced ROS generation and inhibition of mitochondrial complex I activity in PC12 cells in an intensity-dependent manner at 30, 50, and 100 mW/cm(2). Furthermore, LIUS stimulation at 100 mW/cm(2) suppressed inhibition of mitochondrial complex activity byMPP(+) and actually resulted in a decrease of a-synuclein phosphorylation and aggregation induced by MMP+ treatment in PC12 cells. LIUS stimulation also inhibited expression of casein kinase 2 (CK2) that appears to mediate ROS-dependent a-synuclein aggregation. Finally, LIUS stimulation alleviated the death of PC12 cells by MPP+ treatment in an intensity-dependent manner. We, hence, suggest that LIUS stimulation inhibits ROS generation by MPP+ treatment, thereby suppressing a-synuclein aggregation in PC12 cells.
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