PINK1减轻α-突触核蛋白引起的线粒体损伤

doi:10.3969/j.issn.1006-7795.2016.01.014

首都医科大学学报 ›› 2016, Vol. 37 ›› Issue (1): 70-75.doi: 10.3969/j.issn.1006-7795.2016.01.014

PINK1减轻α-突触核蛋白引起的线粒体损伤

王雪, 申甲梅, 高歌, 段春礼, 鲁玲玲, 杨慧

首都医科大学基础医学院神经生物学系北京脑重大疾病研究院帕金森病研究所教育部神经变性病重点实验室, 北京 100069

收稿日期:2015-10-30 出版日期:2016-02-21 发布日期:2016-02-01
通讯作者: 杨慧 E-mail:huiyang@ccmu.edu.cn
基金资助:
国家自然科学基金(81170407,31301154), 北京市属高等学校创新团队建设与教师职业发展计划项目(IDHT20150502)。

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

Wang Xue, Shen Jiamei, Gao Ge, Duan Chunli, Lu Lingling, Yang Hui

Department of Neurobiology, School of Basic Medical Sciences, Capital Medical University, Center for Parkinson's Disease, Beijing Institute for Brain Disorders, Key Laboratory for Neurodegenerative Diseases of the Ministry of Education, Beijing 100069, China

Received:2015-10-30 Online:2016-02-21 Published:2016-02-01
Supported by:
This study was supported by National Natural Science Foundation of China(81170407, 31301154), The Project of Construction of Innovative Teams and Teacher Career Development for Universities and Colleges Under Beijing Municipality(IDHT20150502).

摘要/Abstract

摘要： 目的证明PINK1对α-突触核蛋白(α-synuclein, α-syn)引起的线粒体损伤的影响。方法将携带人源PINK1 和α-syn基因的质粒共转染MN9D多巴胺能神经细胞,流式细胞术检测细胞内活性氧(reactive oxygen species, ROS)、线粒体渗透性转运孔(mitochondrial permeability pore, mPTP)的开放情况及线粒体膜电势(ΔΨ_m)变化;MTT和乳酸脱氢酶法检测细胞活力及细胞损伤情况。结果 PINK1减少α-syn引起的ROS的生成、线粒体膜孔的开放及线粒体膜电势降低,并减轻α-syn所致细胞活力下降及和细胞损伤。结论 PINK1可以减轻α-syn引起的线粒体损伤。

关键词: PINK1, α-突触核蛋白, 线粒体

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

中图分类号:

R741

王雪, 申甲梅, 高歌, 段春礼, 鲁玲玲, 杨慧. PINK1减轻α-突触核蛋白引起的线粒体损伤[J]. 首都医科大学学报, 2016, 37(1): 70-75.

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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PINK1减轻α-突触核蛋白引起的线粒体损伤

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

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