TRIM24 protects cardiomyocyte apoptosis induced by ischemia-reperfusion by inhibiting EndoG nuclear transfer
Wang Sha
Wang Huijun
Huang Xiaoyan
Wang Zongchao
Song Baoguo
Wu Juan
Abstract：To explore the role and molecular mechanism of TRIM24 in ischemia-reperfusion-induced cardiomyocyte apoptosis. Methods A model of H9C2 cardiomyocyte ischemia-reperfusion injury was established. Apoptosis was detected by flow cytometry, and the expression of TRIM24 and apoptosis-related proteins in ischemia-reperfusion-induced cardiomyocyte apoptosis was detected by Western blot. Subsequently, TRIM24 was used to verify its anti-apoptotic effect and molecular mechanism, and the nuclear and cytoplasmic proteins were extracted by nucleocapsid protein isolation kit, and the distribution of EndoG nucleoplasm was detected. Results Ischemia-reperfusion injury induced significantly cardiomyocytes apoptosis, and the expression of TRIM24 was decreased in apoptotic cardiomyocytes. Overexpression of TRIM24 ameliorated mitochondrial homeostasis by regulating the expression of BAX and BCL-2, which could reduce the nucleus translocation of apoptosis-associated protein EndoG from mitochondria. Finally, TRIM24 overexpression significantly reduced cardiomyocytes apoptosis induced by ischemia-reperfusion injury. Conclusion TRIM24 ameliorates mitochondrial homeostasis by regulating the expression of BAX and BCL-2, which could reduce the nucleus translocation of apoptosis-associated protein EndoG from mitochondria, and ultimately reducing cardiomyocytes apoptosis induced by ischemia-reperfusion injury.
Keywords：TRIM24Ischemia-reperfusionCardiomyocytes apoptosisEndoG
Publication Date：2019-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：4( 55-58 )