Abstract:
:Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra. Prevailing evidence suggests that abnormal autophagy and mitochondrial dysfunction participate in the process of PD. However, many damages of neuronal functions are regulated by intracellular Ca2+ signaling and the contribution of mitochondrial Ca2+ to the process of neurodegeneration is still unclear. MPP+, the metabolite of a neurotoxin MPTP, causes symptom of PD in animal models by selectively destroying dopaminergic neurons in substantia nigra. Here we report that mitochondrial Ca2+ uniporter (MCU) participated in MPP+-induced autophagic cell death in SH-SY5Y cells. Pharmacological agonist of MCU or exogenous expressed MCU can partially reduce MPP+-induced autophagic cell death. Down-regulation of MCU enhanced autophagic cell death via AMPK activation, which was independent of Beclin1 and PI3K. These findings show that the mitochondrial calcium dyshomeostasis contributes to MPP+-induced neuronal degeneration, and MCU may be a potential therapeutic target of PD through the prevention of pathological autophagy.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Zhao M,Chen J,Mao K,She H,Ren Y,Gui C,Wu X,Zou F,Li Wdoi
10.1016/j.bbrc.2018.12.148subject
Has Abstractpub_date
2019-02-05 00:00:00pages
390-394issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(18)32817-1journal_volume
509pub_type
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