Mic60/mitofilin overexpression alters mitochondrial dynamics and attenuates vulnerability of dopaminergic cells to dopamine and rotenone
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- 作者：Victor S. Van Laara ; c ; Sarah B. Bermana ; c ; Teresa G. Hastingsa ; b ; c ; hastingst@upmc.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：FCCP ; Carbonyl cyanide-4-(trifluoromethoxy) phenylhydrazone ; DMSO ; dimethyl sulfoxide ; DrOF ; Direct Observation of Fission and Fusion ; DA ; dopamine ; DAQ ; dopamine quinone ; ETC ; electron transport chain ; EV-shRNA ; empty vector pRS plasmid negative control TR20003 ; GFP-shRNA ; GFP-targeted shRNA construct negative control TR30003 ; Mic60&prime ; 05 ; Mic60 targeted shRNA TI348605 ; Mic60&prime ; 07 ; Mic60 targeted shRNA TI348607 ; Mic60&prime ; 08 ; Mic60 targeted shRNA TI348608 ; MICOS ; mitochondrial contact
- 刊名：Neurobiology of Disease
- 出版年：2016
- 出版时间：July 2016
- 年：2016
- 卷：91
- 期：Complete
- 页码：247-261
- 全文大小：3204 K
文摘
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The role of mitochondrial mitofilin (Mic60) in cell vulnerability was examined in models of Parkinson's disease (PD).
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Decreased Mic60 expression increased cellular vulnerability to dopamine (DA)-induced toxicity.
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Mic60 overexpression attenuated cellular vulnerability to DA- and rotenone-induced toxicity.
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Cells overexpressing Mic60 exhibited increased mitochondrial respiratory capacity following low-dose rotenone.
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Neuronal cells overexpressing Mic60 displayed suppressed mitochondrial fission and increased mitochondrial length.