WDR26 promotes mitophagy of cardiomyocytes induced by hypoxia through Parkin translocation

Myocardial ischemia is a heart condition caused by reduction of blood flow to the heart, preventing heart from receiving enough oxygen. Myocardial ischemia is the most common cause of death globally. Heart ischemic preconditioning (IPC) has a protective effect against myocardial cell death induced b...

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Veröffentlicht in:Acta biochimica et biophysica Sinica 2016-12, Vol.48 (12), p.1075-1084
Hauptverfasser: Feng, Yansheng, Zhao, Jia, Hou, Huifang, Zhang, Hui, Jiao, Yunjuan, Wang, Jiangang, Wang, Yongling, Sun, Yinping
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container_issue 12
container_start_page 1075
container_title Acta biochimica et biophysica Sinica
container_volume 48
creator Feng, Yansheng
Zhao, Jia
Hou, Huifang
Zhang, Hui
Jiao, Yunjuan
Wang, Jiangang
Wang, Yongling
Sun, Yinping
description Myocardial ischemia is a heart condition caused by reduction of blood flow to the heart, preventing heart from receiving enough oxygen. Myocardial ischemia is the most common cause of death globally. Heart ischemic preconditioning (IPC) has a protective effect against myocardial cell death induced by ischemia and ischemia-reperfusion injury. WDR26 has recently been identified as a protein that is increased following rat cardiac IPC. WDR26 can promote the proliferation of H9c2 cells and protect cardiomyocytes against oxidative stress through inhibiting apoptosis. However, its role in myocardial ischemia is unclear. The aim of this study was to explore the role of WDR26 in myocardial ischemia and H9c2 cell hypoxia. Our results showed that WDR26 is induced by myocardial ischemia and H9c2 cell hypoxia. WDR26 protects H9c2 cells against hypoxia injury through inhibiting LDH release and increasing cell viability. WDR26 promotes hypoxia-induced autophagy in hypoxia of H9c2 cells. We further demonstrated that in H9c2 cell hypoxia, WDR26 increases mitochondrial membrane potential, thereby increases Parkin translocation of mitochondria. After Parkin is translocated at mitochondria, WDR26 can increase mitochondrial protein ubiquitination in hypoxia of H9c2 cells. WDR26 is a mediator of response to hypoxia, and WDR26 plays an important role in hypoxia-mediated autophagy and mitophagy. This study provides novel insights into the protective role of WDR26 in cardiomyocyte injury during hypoxia. WDR26 may serve as a potential target for the treatment of myocardial ischemia.
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Myocardial ischemia is the most common cause of death globally. Heart ischemic preconditioning (IPC) has a protective effect against myocardial cell death induced by ischemia and ischemia-reperfusion injury. WDR26 has recently been identified as a protein that is increased following rat cardiac IPC. WDR26 can promote the proliferation of H9c2 cells and protect cardiomyocytes against oxidative stress through inhibiting apoptosis. However, its role in myocardial ischemia is unclear. The aim of this study was to explore the role of WDR26 in myocardial ischemia and H9c2 cell hypoxia. Our results showed that WDR26 is induced by myocardial ischemia and H9c2 cell hypoxia. WDR26 protects H9c2 cells against hypoxia injury through inhibiting LDH release and increasing cell viability. WDR26 promotes hypoxia-induced autophagy in hypoxia of H9c2 cells. We further demonstrated that in H9c2 cell hypoxia, WDR26 increases mitochondrial membrane potential, thereby increases Parkin translocation of mitochondria. After Parkin is translocated at mitochondria, WDR26 can increase mitochondrial protein ubiquitination in hypoxia of H9c2 cells. WDR26 is a mediator of response to hypoxia, and WDR26 plays an important role in hypoxia-mediated autophagy and mitophagy. This study provides novel insights into the protective role of WDR26 in cardiomyocyte injury during hypoxia. WDR26 may serve as a potential target for the treatment of myocardial ischemia.</description><identifier>ISSN: 1672-9145</identifier><identifier>EISSN: 1745-7270</identifier><identifier>DOI: 10.1093/abbs/gmw104</identifier><identifier>PMID: 27797717</identifier><language>eng</language><publisher>China</publisher><subject>Animals ; Cell Hypoxia ; Cell Line ; Membrane Potential, Mitochondrial ; Mitochondrial Degradation - physiology ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - metabolism ; Protein Transport ; Proteins - physiology ; Rats ; Rats, Sprague-Dawley ; Ubiquitin-Protein Ligases - metabolism ; 心肌细胞损伤 ; 心肌缺血 ; 易位 ; 线粒体膜电位 ; 细胞缺氧 ; 缺血再灌注损伤 ; 自噬 ; 诱导</subject><ispartof>Acta biochimica et biophysica Sinica, 2016-12, Vol.48 (12), p.1075-1084</ispartof><rights>The Author 2016. Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. 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We further demonstrated that in H9c2 cell hypoxia, WDR26 increases mitochondrial membrane potential, thereby increases Parkin translocation of mitochondria. After Parkin is translocated at mitochondria, WDR26 can increase mitochondrial protein ubiquitination in hypoxia of H9c2 cells. WDR26 is a mediator of response to hypoxia, and WDR26 plays an important role in hypoxia-mediated autophagy and mitophagy. This study provides novel insights into the protective role of WDR26 in cardiomyocyte injury during hypoxia. 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subjects Animals
Cell Hypoxia
Cell Line
Membrane Potential, Mitochondrial
Mitochondrial Degradation - physiology
Myocytes, Cardiac - cytology
Myocytes, Cardiac - metabolism
Protein Transport
Proteins - physiology
Rats
Rats, Sprague-Dawley
Ubiquitin-Protein Ligases - metabolism
心肌细胞损伤
心肌缺血
易位
线粒体膜电位
细胞缺氧
缺血再灌注损伤
自噬
诱导
title WDR26 promotes mitophagy of cardiomyocytes induced by hypoxia through Parkin translocation
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