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CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain

文献类型：期刊论文

作者Zuo, Shengkai1,2; Kong, Deping1; Wang, Yuanyang1; Zhang, Jian1; Li, Xin1; Shen, Yujun1; Yu, Ying1,2; Wang, Chenyao2; Liu, Jiao2; Wan, Qiangyou2
刊名EMBO MOLECULAR MEDICINE
出版日期2018
卷号10期号:3页码:UNSP e8237
关键词calpain cardiomyocyte apoptosis CRTH2 endoplasmic reticulum stress prostaglandin D-2
ISSN号1757-4676
DOI10.15252/emmm.201708237
文献子类Article
英文摘要Apoptotic death of cardiac myocytes is associated with ischemic heart disease and chemotherapy-induced cardiomyopathy. Chemoattractant receptor-homologous molecule expressed on T helper type 2 cells (CRTH2) is highly expressed in the heart. However, its specific role in ischemic cardiomyopathy is not fully understood. Here, we demonstrated that CRTH2 disruption markedly improved cardiac recovery in mice postmyocardial infarction and doxorubicin challenge by suppressing cardiomyocyte apoptosis. Mechanistically, CRTH2 activation specifically facilitated endoplasmic reticulum (ER) stress-induced cardiomyocyte apoptosis via caspase-12-dependent pathway. Blockage of m-calpain prevented CRTH2-mediated cardiomyocyte apoptosis under ER stress by suppressing caspase-12 activity. CRTH2 was coupled with G(q) to elicit intracellular Ca2+ flux and activated m-calpain/caspase-12 cascade in cardiomyocytes. Knockdown of caspase-4, an alternative to caspase-12 in humans, markedly alleviated CRHT2 activation-induced apoptosis in human cardiomyocyte response to anoxia. Our findings revealed an unexpected role of CRTH2 in promoting ER stress-induced cardiomyocyte apoptosis, suggesting that CRTH2 inhibition has therapeutic potential for ischemic cardiomyopathy.
学科主题Research & Experimental Medicine
WOS关键词ACUTE MYOCARDIAL-INFARCTION ; PROSTAGLANDIN D-2 RECEPTOR ; INDUCED CELL-DEATH ; HEART-FAILURE ; CARDIAC-HYPERTROPHY ; IN-VITRO ; 15-DEOXY-DELTA(12,14)-PROSTAGLANDIN J(2) ; VENTRICULAR FUNCTION ; MEDIATED APOPTOSIS ; REPERFUSION INJURY
语种英语
WOS记录号WOS:000426769000007
出版者WILEY
版本出版稿
源URL[http://202.127.25.144/handle/331004/1016]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Tianjin Med Univ, Dept Pharmacol, Key Lab Immune Microenvironm & Dis, Sch Basic Med Sci,Minist Educ, Tianjin, Peoples R China;
2.Chinese Acad Sci, Key Lab Food Safety Res, Inst Nutr Sci, Shanghai Inst Biol Sci, Shanghai, Peoples R China;
3.Univ Miami, Coll Arts & Sci, Dept Biol, Miami, FL USA;
4.Guangdong Acad Med Sci, Guangdong Gen Hosp, Guangdong Cardiovasc Inst, Guangdong Acad Med Sci,Med Res Dept, Guangzhou, Guangdong, Peoples R China;
5.Univ N Carolina, McAllister Heart Inst, Chapel Hill, NC USA,
推荐引用方式
GB/T 7714		 Zuo, Shengkai,Kong, Deping,Wang, Yuanyang,et al. CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain[J]. EMBO MOLECULAR MEDICINE,2018,10(3):UNSP e8237.
APA Zuo, Shengkai.,Kong, Deping.,Wang, Yuanyang.,Zhang, Jian.,Li, Xin.,...&,.(2018).CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain.EMBO MOLECULAR MEDICINE,10(3),UNSP e8237.
MLA Zuo, Shengkai,et al."CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain".EMBO MOLECULAR MEDICINE 10.3(2018):UNSP e8237.

入库方式： OAI收割

来源：上海营养与健康研究所

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