期刊
MOLECULAR NEUROBIOLOGY
卷 54, 期 8, 页码 6107-6119出版社
SPRINGER
DOI: 10.1007/s12035-016-0145-3
关键词
TUDCA; Mitochondria; Autophagy; Mitophagy; Parkin; SH-SY5Y cells
资金
- Fundacao para a Ciencia e a Tecnologia (FCT), Portugal [UID/DTP/04138/2013, PTDC/NEU-NMC/0248/2012, PTDC/NEU-OSD/0502/2012, SFRH/BPD/95855/2013]
- Fundação para a Ciência e a Tecnologia [SFRH/BPD/95855/2013, PTDC/NEU-OSD/0502/2012, PTDC/NEU-NMC/0248/2012] Funding Source: FCT
Mitochondrial dysfunction has been deeply implicated in the pathogenesis of several neurodegenerative diseases. Thus, to keep a healthy mitochondrial population, a balanced mitochondrial turnover must be achieved. Tauroursodeoxycholic acid (TUDCA) is neuroprotective in various neurodegenerative disease models; however, the mechanisms involved are still incompletely characterized. In this study, we investigated the neuroprotective role of TUDCA against mitochondrial damage triggered by the mitochondrial uncoupler carbonyl cyanide m-chlorophelyhydrazone (CCCP). Herein, we show that TUDCA significantly prevents CCCP-induced cell death, ROS generation, and mitochondrial damage. Our results indicate that the neuroprotective role of TUDCA in this cell model is mediated by parkin and depends on mitophagy. The demonstration that pharmacological up-regulation of mitophagy by TUDCA prevents neurodegeneration provides new insights for the use of TUDCA as a modulator of mitochondrial activity and turnover, with implications in neurodegenerative diseases.
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