title: MTERF2 contributes to MPP(+)-induced mitochondrial dysfunction and cell damage.
abstract: Parkinson's disease (PD) is a common neurodegenerative disorder whose pathogenesis is under intense investigation. Substantial evidence indicates that mitochondrial dysfunction plays a central role in the pathophysiology of PD. Several mitochondrial internal regulating factors act to maintain the mitochondrial function. However, how these internal regulating factors contribute to mitochondrial dysfunction in PD remains elusive. One of these factors, mitochondrial transcription termination factor 2 (MTERF2), has been implicated in the regulation of oxidative phosphorylation by modulating mitochondrial DNA transcription. Here, we discovered a new role of MTERF2 in regulating mitochondrial dysfunction and cell damage induced by MPP(+) in SH-SY5Y cells. We found that MPP(+) treatment elevated MTERF2 expression, induced mitochondrial dysfunction and cell damage, which was alleviated by MTERF2 knockdown. These findings demonstrate that MTERF2 contributes to MPP(+)-induced mitochondrial disruption and cell damage. This study indicates that MTERF2 is a potential therapeutic target for environmentally induced Parkinson's disease.
authors.affiliation: Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
authors.forename: Yanyan
authors.initials: Y
authors.lastname: Han
authors.affiliation: Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
authors.forename: Peiye
authors.initials: P
authors.lastname: Gao
authors.affiliation: Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
authors.forename: Shi
authors.initials: S
authors.lastname: Qiu
authors.affiliation: Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
authors.forename: Linbing
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Yang
authors.affiliation: Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
authors.forename: Ji
authors.initials: J
authors.lastname: Zuo
authors.affiliation: State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
authors.forename: Chunjiu
authors.initials: C
authors.lastname: Zhong
authors.affiliation: Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. Electronic address: shun_zhu@fudan.edu.cn.
authors.forename: Shun
authors.initials: S
authors.lastname: Zhu
authors.affiliation: Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. Electronic address: liuwen@shmu.edu.cn.
authors.forename: Wen
authors.initials: W
authors.lastname: Liu
mesh_terms: D015655:1-Methyl-4-phenylpyridinium; D002460:Cell Line; D004268:DNA-Binding Proteins; D006801:Humans; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D024101:Mitochondrial Proteins / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D020734:Parkinsonian Disorders / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D014157:Transcription Factors / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D004268:DNA-Binding Proteins; C506545:MTERF2 protein, human; D024101:Mitochondrial Proteins; D014157:Transcription Factors; D015655:1-Methyl-4-phenylpyridinium
keywords: CCCP; MPP(+); Mitochondrial dysfunction; Mitochondrial transcription termination factors 2 (MTERF2); Parkinson's disease; Protein transport