MFN1介导的线粒体融合在心肌细胞凋亡中的作用研究

目的:探讨线粒体融合关键蛋白MFN1介导的线粒体融合在调控心肌细胞凋亡中的作用。方法:通过si RNA降低体外培养H9C2心肌细胞中MFN1的表达后,采用Western blot检测线粒体细胞色素c(Cyto c)释放及其下游凋亡效应分子Caspase9与Caspase3活性,流式细胞术检测细胞内活性氧(ROS)的产生情况,流式细胞术检测细胞凋亡的情况。结果:干扰MFN1可显著促进H9C2心肌细胞内细胞色素c由线粒体释放至胞浆,促进Caspase9与Caspase3的激活,增加细胞内活性氧ROS产生并提高细胞凋亡率(均P0.05)。结论:MFN1介导的线粒体融合可保护心肌细胞凋亡,其机制可能与抑制ROS产生与细胞色素C释放有关。

Effect of MFN1 Mediated Mitochondrial Fusion on the Apoptosis of H9C2 Cardiomyocytes

ABSTRACT Objective: To investigate the role of MFN1-mediated mitochondrial fusion in the regulation of cardiomyocyte apoptosis. Methods: After knocking down of MFN1 with siRNA in H9C2 cardiomyocytes, cytochrome c release, caspase9 and caspase3 activation, intracellular ROS and cell apoptosis were evaluated by western blotting and flow cytometry. Results: 1). MFN1 significantly promoted the release of cytochrome cfrom the mitochondria to the cytosol, activation of caspase9 and caspase3 ROS production and apoptosis of H9C2 cardiomyocytes (all P<0.05). Conclusion: MFN1-mediated mitochondrial fusion protects cardiomyocyte from apoptosis, which could be partially explained by the inhibition of ROS production and cytochrome c release.