Molecular effects of activated BV-2 microglia by mitochondrial toxin 1-methyl-4-phenylpyridinium
- 作者：Meihua Jin1 ; Byung Wook Kim1 ; Sushruta Koppula ; In Su Kim ; Ji-Hwan Park ; Hemant Kumar ; Dong-Kug Choi ; choidk@kku.ac.kr
- 关键词：CD68 ; cluster of differentiation 68 ; FACS ; registered trademark of Becton Dickinson and Company ; FITC ; fluorescein isothiocyanate ; GAPDH ; glyceraldehyde 3-phosphate dehydrogenase ; MAC-1 ; macrophage antigen complex-1 ; MPP+ ; 1-methyl-4-phenylpyridinium ; MPT
- 刊名：Neurotoxicology
- 出版年：2012
- 期刊代码：35_0161813x
- 类别：pha
- 出版时间：March, 2012
- 卷：33
- 期：2
- 页码：147-155
- 文件大小：1111 K
摘要
Microglia plays an important role in inflammation-mediated neurodegeneration. Compelling evidence supports the hypothesis that microglial activation contributes to the pathogenesis of various neurodegenerative diseases. However, little is known about the molecular outcome of activated microglia. In this report, we investigate the molecular consequences of MPP+ toxin-induced activated BV-2 microglia. Intoxication of specific mitochondrial toxin methyl-4-phenylpyridinium iodide ion (MPP+) to BV-2 cells induced significant mitochondrial dysfunction and increased the reactive oxygen species generation, caspase-3 activation, and poly ADP ribose polymerase proteolysis. Further, MAC-1 immunostaining in the midbrain of mice revealed a decrease in activated microglia at day 4 after intoxication with MPP+. From this study, it was confirmed that BV-2 microglia respond to the mitochondrial toxin MPP+ which may lead to apoptotic cell death. Understanding of the mechanistic basis of apoptotic elimination of activated microglia may help to develop new strategies for the treatment of neurodegenerative diseases.