scholarly journals Involvement of Tumor Necrosis Factor Receptor-associated Protein 1 (TRAP1) in Apoptosis Induced by β-Hydroxyisovalerylshikonin

2004 ◽  
Vol 279 (41) ◽  
pp. 42503-42515 ◽  
Author(s):  
Yutaka Masuda ◽  
Genryu Shima ◽  
Toshihiro Aiuchi ◽  
Masayo Horie ◽  
Kouichi Hori ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Associated Protein ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a mitochondria-dependent pathway mediated by cytochrome c oxidase subunit II

2019 ◽  
Vol 7 ◽  
Author(s):  
Fei Xiang ◽  
Si-yuan Ma ◽  
Yan-ling Lv ◽  
Dong-xia Zhang ◽  
Hua-pei Song ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Necrosis Factor ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Cardiomyocyte Apoptosis ◽  
Oxygen Species ◽  
Receptor Associated Protein ◽  
Necrosis Factor

Abstract Background Tumor necrosis factor receptor-associated protein 1 (TRAP1) plays a protective effect in hypoxic cardiomyocytes, but the precise mechanisms are not well clarified. The study is aimed to identify the mechanism of TRAP1 on hypoxic damage in cardiomyocytes. Methods 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 separately. Results Hypoxia induced cardiomyocyte apoptosis, and TRAP1 overexpression notably inhibited apoptosis induced by hypoxia. Conversely, TRAP1 silencing promoted apoptosis in hypoxic cardiomyocytes. Further 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 overexpression. Additionally, 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 apoptosis. Conclusions 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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