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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.
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页码:464 / 469
页数:6
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