TRPC3 participates in α-synuclein-induced mitochondrial damage

doi:10.3969/j.issn.1006-7795.2017.06.016

Abstract

Abstract: Objective To investigate the role of transient receptor potential canonical channel 3 (TRPC3)in the mitochondrial damage induced by aberrant α-synuclein (α-syn) accumulation.Methods Expressions of TRPC3 and α-syn in mitochondria were detected by Western blotting and immunofluorescence in α-syn-overexpressing primary neurons and α-syn transgenic and knock-out mice.The detection of mitochondrial membrane potential(MMP) by JC-1 showed mitochondrial damage and the detection of cell viability used MTT and lactated dehydrogenase(LDH) release assays in α-syn-overexpression primary neurons which TRPC3 was knocked down.Results TRPC3 and α-syn co-expressed in mitochondria. Neurons overexpressing α-syn increased mitochondrial TRPC3 expression and decreased MMP and cell viability. Suppressing TRPC3 expression partially reversed the α-syn-induced reductions in MMP and cell viability.Conclusion Mitochondrial TRPC3 may participate in α-syn-induced mitochondrial damage.

Key words: Parkinson's disease, neuron, α-synuclein, transient receptor potential canonical channel 3(TRPC3), mitochondria

CLC Number:

Q189

Lu Yongquan, Chen Min, Gao Ge, Duan Chunli, Lu Lingling, Yang Hui. TRPC3 participates in α-synuclein-induced mitochondrial damage[J]. Journal of Capital Medical University, 2017, 38(6): 857-862.

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URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2017.06.016

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2017/V38/I6/857

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