Peroxiredoxin 5 prevents amyloid-beta oligomer-induced neuronal cell death by inhibiting ERK-Drp1-mediated mitochondrial fragmentation
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- 作者：Bokyung Kima ; 1 ; Junghyung Parka ; 1 ; Kyu-Tae Changb ; Dong-Seok Leea ; lee1@knu.ac.kr" class="auth_mail" title="E-mail the corresponding author
- 关键词：AβO ; amyloid-beta oligomer ; AD ; Alzheimer's disease ; COX IV ; cytochrome c oxidase IV ; DMSO ; dimethyl sulfoxide ; Drp1 ; dynamin related protein ; DsRed2 ; Discosoma red fluorescent protein ; ERK ; extracellular signal-regulated kinase ; GAPDH ; glyceraldehyde 3-phosphate dehydrogenase ; MTT ; 3-(4 ; 5-dimethyl-2-thiazolyl)-2 ; 5-diphenyl-2H-tetrazolium bromide ; NAC ; N-acetyl-l-cysteine ; Prx ; peroxiredoxin ; RNS ; reactive nitrogen species ; ROS ; reactive oxygen species
- 刊名：Free Radical Biology and Medicine
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：90
- 期：Complete
- 页码：184-194
- 全文大小：3093 K
文摘
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Prx5 expression was upregulated by AβO-induced oxidative stress.
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Prx5 ameliorated AβO-induced phosphorylation of Drp1-Ser616.
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AβO-induced phosphorylation of Drp1-Ser616 increased mitochondrial fragmentation.
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Prx5 ameliorated ERK phosphorylation by reducing AβO-induced oxidative stress.
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Apoptotic cell death was decreased by Prx5.