1. Academic Validation
  2. WDR26 promotes mitophagy of cardiomyocytes induced by hypoxia through Parkin translocation

WDR26 promotes mitophagy of cardiomyocytes induced by hypoxia through Parkin translocation

  • Acta Biochim Biophys Sin (Shanghai). 2016 Dec;48(12):1075-1084. doi: 10.1093/abbs/gmw104.
Yansheng Feng 1 Jia Zhao 1 Huifang Hou 1 2 Hui Zhang 3 Yunjuan Jiao 4 5 Jiangang Wang 1 Yongling Wang 6 Yinping Sun 6
Affiliations

Affiliations

  • 1 Department of Pathophysiology, Xinxiang Medical University, Xinxiang 453003, China.
  • 2 Department of Pathophysiology, West China School of Preclinical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, China.
  • 3 School of Nursing, Xinxiang Medical University, Xinxiang 453003, China.
  • 4 Department of Pathology, Xinxiang Medical University, Xinxiang 453003, China.
  • 5 Department of Histology and Embryology, School of Basic Medical Sciences, Central South University, Changsha 410008, China.
  • 6 Department of Pathophysiology, Xinxiang Medical University, Xinxiang 453003, China 011025@xxmu.edu.cn sypxxmu@sina.com.
Abstract

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.

Keywords

WDR26; autophagy; hypoxia; mitophagy; myocardial ischemia.

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