Study of PINK1 rescuing the mitochondrial dysfunction induced by α-synuclein

doi:10.3969/j.issn.1006-7795.2016.01.014

Abstract

Abstract: Objective To identify whether PINK1 could rescue the mitochondrial dysfunction induced by α-synuclein. Methods MN9D cells were transfected with plasmid encoding human α-synuclein together with human wild type PINK1. The level of reactive oxygen species (ROS), mitochondrial permeability pore (mPTP) and mitochondrial membrane potential (ΔΨm) were examined by flow cytometry. The cell viability was observed by MTT assay and release of lactate dehydrogenase(LDH) respectively. Results While overexpression PINK1 could ease the opening of mPTP, reducing the generation of ROS, ΔΨm reduction percentage reduction by α-syn, reversed α-syn decreased cell viability and induced LDH release by α-syn induced. Conclusion PINK1 could alleviate α-syn-induced mitochondrial injury.

Key words: PINK1, α-synuclein (α-syn), mitochondria

CLC Number:

R741

Wang Xue, Shen Jiamei, Gao Ge, Duan Chunli, Lu Lingling, Yang Hui. Study of PINK1 rescuing the mitochondrial dysfunction induced by α-synuclein[J]. Journal of Capital Medical University, 2016, 37(1): 70-75.

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URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2016.01.014

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2016/V37/I1/70

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