Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a mitochondria-dependent pathway mediated by cytochrome c oxidase subunit Ⅱ
作者机构：Institute of Burn ResearchState Key Laboratory of TraumaBurns and Combined InjurySouthwest HospitalThird Military Medical University(Army Medical University)Chongqing 400038China
出 版 物：《Burns & Trauma》 (烧伤与创伤（英文）)
年 卷 期：2019年第7卷第1期
页 面：139-149页
核心收录：
学科分类：0831[工学-生物医学工程（可授工学、理学、医学学位）] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 1011[医学-护理学（可授医学、理学学位）] 100214[医学-肿瘤学] 0836[工学-生物工程] 10[医学]
基 金：supported by the National Natural Science Foundation of China(NSFC)(Grant No:81101426 81571898)
主 题：Cardiomyocytes Hypoxia Tumor necrosis factor receptor-associated protein 1 Cytochrome c oxidase subunitⅡ Reactive oxygen species Apoptosis
摘 要：Background:Tumor necrosis factor receptor-associated protein 1(TRAP1)plays a protective effect in hypoxic cardiomyocytes,but the precise mechanisms are not well *** study is aimed to identify the mechanism of TRAP1 on hypoxic damage in ***:In this study,the effects of TRAP1 and cytochrome c oxidase subunit Ⅱ(COXⅡ)on apoptosis in hypoxia-induced cardiomyocytes were explored using overexpression and knockdown methods ***:Hypoxia induced cardiomyocyte apoptosis,and TRAP1 overexpression notably inhibited apoptosis induced by ***,TRAP1 silencing promoted apoptosis in hypoxic *** investigation revealed that the proapoptotic effects caused by the silencing of TRAP1 were prevented by COXⅡ overexpression,whereas COXⅡ knockdown reduced the antiapoptotic function induced by TRAP1 ***,changes in the release of cytochrome c from mitochondria into the cytosol and the caspase-3 activity in the cytoplasm,as well as reactive oxygen species production,were found to be correlated with the changes in ***:The current study uncovered that TRAP1 regulates hypoxia-induced cardiomyocyte apoptosis through a mitochondria-dependent apoptotic pathway mediated by COXⅡ,in which reactive oxygen species presents as an important component.
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