典型文献
MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells
文献摘要:
Parkinson's disease(PD)is a neurodegenerative disorder causing severe social and economic burdens.The origin of PD has been usually attributed to mitochondrial dysfunction.To this end,mitochondrial transcription regulators become attractive subjects for understanding PD pathogenesis.Previously,we found that the expression of mi-tochondrial transcription termination factor 3(MTERF3)was reduced in MPP+-induced mice model of PD.In the present study,we probe the function of MTERF3 and its role in MPP+-induced cellular model of PD.Initially,we observe that MTERF3 expression is also reduced in MPP+-induced cellular model of PD,which can be mainly attributed to the increase of MTERF3 degradation.Next,we examine the effect of MTERF3 knockdown and over-expression on the replication,transcription,and translation of mitochondrial DNA(mtDNA).We show that knock-down and overexpression of MTERF3 have opposite effects on mtDNA transcript level but similar effects on mtDNA expression level,in line with MTERF3's dual roles in mtDNA transcription and translation.In addition,we examine the effect of MTERF3 knockdown and overexpression on mitochondrial function with and without MPP+treatment,and find that MTERF3 seems to play a generally protective role in MPP+-induced mitochondrial dysfunction.Together,this work suggests a regulatory role of MTERF3 in MPP+-induced cellular model of PD and may provide clues in designing novel therapeutics against PD.
文献关键词:
中图分类号:
作者姓名:
Shun Zhu;Nan Xu;Yanyan Han;Xiaofei Ye;Ling Yang;Ji Zuo;Wen Liu
作者机构:
Department of Cellular and Genetic Medicine,School of Basic Medical Sciences,Fudan University,Shanghai 200032,China
文献出处:
引用格式:
[1]Shun Zhu;Nan Xu;Yanyan Han;Xiaofei Ye;Ling Yang;Ji Zuo;Wen Liu-.MTERF3 contributes to MPP+-induced mitochondrial dysfunction in SH-SY5Y cells)[J].生物化学与生物物理学报(英文版),2022(08):1113-1121
A类:
MTERF3,MPP+treatment
B类:
contributes,induced,mitochondrial,dysfunction,SH,SY5Y,cells,Parkinson,disease,neurodegenerative,disorder,causing,severe,social,economic,burdens,origin,has,been,usually,attributed,this,end,transcription,regulators,become,attractive,subjects,understanding,pathogenesis,Previously,we,found,that,termination,was,reduced,mice,model,present,study,probe,its,cellular,Initially,observe,also,which,can,mainly,increase,degradation,Next,examine,knockdown,replication,translation,mtDNA,We,show,overexpression,have,opposite,effects,level,similar,line,dual,roles,addition,without,find,seems,play,generally,protective,Together,work,suggests,regulatory,may,provide,clues,designing,novel,therapeutics,against
AB值:
0.422151
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