Neuregulin-1 protects myocardial cells against H2O2-induced apoptosis by regulating endoplasmic reticulum stress

被引:16
|
作者
Xu, Min [1 ]
Wu, Xuesi [1 ]
Jie, Bingzhang [2 ]
Zhang, Xiaoxia [1 ]
Zhang, Jinglan [1 ]
Xin, Yi [1 ]
Guo, Yongfang [3 ]
机构
[1] Capital Med Univ, Beijing Anzhen Hosp, Beijing Inst Heart Lung & Blood Vessel Dis, Beijing 100029, Peoples R China
[2] Beijing Fuxing Hosp, Dept Cardiol, Beijing, Peoples R China
[3] Qingdao Univ, Coll Med, Affiliated Hosp, Dept Cardiol, Qingdao 266071, Shandong, Peoples R China
基金
北京市自然科学基金;
关键词
neuregulin; apoptosis; cardiac myocyte; endoplasmic reticulum stress; OXIDATIVE STRESS; HEART-FAILURE; CARDIOMYOCYTES; THERAPY; PATHWAY;
D O I
10.1002/cbf.3038
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Neuregulin-1 (NRG-1) is a stress-mediated growth factor secreted by cardiovascular endothelial cells and provides the protection to myocardial cells, but the underlying mechanisms are not fully understood. This study aimed to demonstrate that NRG-1 protects myocardial cells exposed to oxidative damage by regulating endoplasmic reticulum (ER) stress. Neonatal rat cardiac myocytes (NRCMs) were isolated and treated with H2O2 as a cellular model of ER stress. NRCMs were pretreated with different concentrations of NRG-1. We found that NRG-1 increased the viability and reduced the apoptosis of NRCMs treated by H2O2. Moreover, NRG-1 reduced lactate dehydrogenase level, increased superoxide dismutase activity and decreased malondialdehyde content in NRCMs treated by H2O2. Finally, we demonstrated that NRG-1 alleviated ER stress and decreased CHOP and GRP78 protein levels in NRCMs treated by H2O2. Taken together, these data indicate that NRG-1 relieves oxidative and ER stress in NRCMs and suggest that NRG-1 is a promising agent for cardioprotection. Copyright (C) 2014 John Wiley & Sons, Ltd.
引用
收藏
页码:464 / 469
页数:6
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