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首页> 外文期刊>Journal of receptor and signal transduction research >Tissue transglutaminase 2 promotes apoptosis of rat neonatal cardiomyocytes under oxidative stress
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Tissue transglutaminase 2 promotes apoptosis of rat neonatal cardiomyocytes under oxidative stress

机译:组织转谷氨酰胺酶2在氧化应激下促进大鼠新生心肌细胞凋亡

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摘要

The role of tissue transglutaminase 2 (TG2) in cardiac myocyte apoptosis under oxidative stress induced by ischemic injury remains unclear. Here, we investigated the effects of TG2 on apoptosis of cardiomyocytes under oxidative stress. Ectopic expression of TG2 increased caspase-3 activity and calcium overload in cardiomyocytes. Expression levels of TG2 were significantly increased in H_2O_2-treated cardiomyocytes. Caspase-3 activity assay demonstrated its considerable correlation with TG2 expression, which supported that caspase-3 inhibitor inhibited the apoptosis induced by the ectopic overexpression of TG2. In addition, the other apoptotic signals, such as caspase-8, cytochrome c, and Bax, were increased dependent with TG2 expression in H_2O_2-treated cardiomyocytes. These results indicated that apoptotic signals had a positive correlation with TG2 expression. The decreased expression of phospholipase C (PLC)-δ1 and phospho-PKC in H _2O_2-treated cardiomyocytes were rescued by TG2 silencing. Together, our data strongly suggest that oxidative stress up-regulates TG2 expression in cardiomyocytes, leading to apoptosis.
机译:尚不清楚组织转谷氨酰胺酶2(TG2)在缺血性损伤引起的氧化应激下心肌细胞凋亡中的作用。在这里,我们调查了TG2对氧化应激下心肌细胞凋亡的影响。 TG2的异位表达增加了心肌细胞中caspase-3的活性和钙超载。在H_2O_2处理的心肌细胞中TG2的表达水平显着增加。 Caspase-3活性测定显示其与TG2表达有显着相关性,这表明caspase-3抑制剂抑制了TG2异位表达所诱导的凋亡。此外,依赖于H_2O_2处理的心肌细胞中TG2的表达,其他凋亡信号(例如半胱天冬酶8,细胞色素c和Bax)增加。这些结果表明凋亡信号与TG2表达呈正相关。 TG2沉默可以挽救H _2O_2处理过的心肌细胞中磷脂酶C(PLC)-δ1和磷酸化PKC的表达降低。总之,我们的数据强烈表明氧化应激会上调心肌细胞中TG2的表达,从而导致细胞凋亡。

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