IR@PKUHSC  > 北京大学基础医学院
学科主题基础医学
Catestatin attenuates endoplasmic reticulum induced cell apoptosis by activation type 2 muscarinic acetylcholine receptor in cardiac ischemia/reperfusion
Liao, Feng1; Zheng, Yang1; Cai, Junyan1; Fan, Jinghui1; Wang, Jing1; Yang, Jichun1,2; Cui, Qinghua1,2; Xu, Guoheng1; Tang, Chaoshu1; Geng, Bin1,2
刊名SCIENTIFIC REPORTS
2015-11-16
DOI10.1038/srep16590
5
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]CHROMOGRANIN-A FRAGMENT ; ACUTE MYOCARDIAL-INFARCTION ; CATECHOLAMINE RELEASE ; BLOOD-PRESSURE ; HEART-FAILURE ; UP-REGULATION ; ER STRESS ; RAT-HEART ; PEPTIDE ; MITOCHONDRIAL
英文摘要

Catestatin (CST) is a catecholamine secretion inhibiting peptide as non-competitive inhibitor of nicotinic acetylcholine receptor. CST play a protective role in cardiac ischemia/reperfusion (I/R) but the molecular mechanism remains unclear. Cardiomyocytes endogenously produced CST and its expression was reduced after I/R. CST pretreatment decreased apoptosis especially endoplasmic reticulum (ER) stress response during I/R. The protection of CST was confirmed in H9c2 cardiomyoblasts under Anoxia/reoxygenation (A/R). In contrast, siRNA-mediated knockdown of CST exaggerated ER stress induced apoptosis. The protective effects of CST were blocked by extracellular signal-regulated kinases 1/2 (ERK1/2) inhibitor PD90895 and phosphoinositide 3-kinase (PI3 K) inhibitor wortmannin. CST also increased ERK1/2 and protein kinase B (Akt) phosphorylation and which was blocked by atropine and selective type 2 muscarinic acetylcholine (M2) receptor, but not type 1 muscarinic acetylcholine (M1) receptor antagonist. Receptor binding assay revealed that CST competitively bound to the M2 receptor with a 50% inhibitory concentration of 25.7 nM. Accordingly, CST inhibited cellular cAMP stimulated by isoproterenol or forskolin, and which was blocked by selective M2 receptor antagonist. Our findings revealed that CST binds to M2 receptor, then activates ERK1/2 and PI3 K/Akt pathway to inhibit ER stress-induced cell apoptosis resulting in attenuation cardiac I/R injury.

语种英语
WOS记录号WOS:000364670400002
项目编号2012CB517806 ; 2012CB517504 ; 81170235 ; 81470552 ; 91339106 ; 81422006
资助机构Major State Basic Research Development Program of the People&prime ; s Republic of China ; National Natural Science Foundation of the People&prime ; s Republic China
引用统计
被引频次:11[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/59566
专题北京大学基础医学院
作者单位1.Peking Univ, Dept Physiol & Pathophysiol, Sch Basic Med Sci, Beijing 100191, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Ctr Noncoding RNA Med, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Liao, Feng,Zheng, Yang,Cai, Junyan,et al. Catestatin attenuates endoplasmic reticulum induced cell apoptosis by activation type 2 muscarinic acetylcholine receptor in cardiac ischemia/reperfusion[J]. SCIENTIFIC REPORTS,2015,5.
APA Liao, Feng.,Zheng, Yang.,Cai, Junyan.,Fan, Jinghui.,Wang, Jing.,...&Geng, Bin.(2015).Catestatin attenuates endoplasmic reticulum induced cell apoptosis by activation type 2 muscarinic acetylcholine receptor in cardiac ischemia/reperfusion.SCIENTIFIC REPORTS,5.
MLA Liao, Feng,et al."Catestatin attenuates endoplasmic reticulum induced cell apoptosis by activation type 2 muscarinic acetylcholine receptor in cardiac ischemia/reperfusion".SCIENTIFIC REPORTS 5(2015).
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