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首页> 外文期刊>Molecular and Cellular Biology >Gene 33/RALT Is Induced by Hypoxia in Cardiomyocytes, Where It Promotes Cell Death by Suppressing Phosphatidylinositol 3-Kinase and Extracellular Signal-Regulated Kinase Survival Signaling
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Gene 33/RALT Is Induced by Hypoxia in Cardiomyocytes, Where It Promotes Cell Death by Suppressing Phosphatidylinositol 3-Kinase and Extracellular Signal-Regulated Kinase Survival Signaling

机译：基因33 / RALT是由缺氧诱导的心肌细胞，通过抑制磷脂酰肌醇3-激酶和细胞外信号调节的激酶存活信号来促进细胞死亡。

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摘要

Ischemia in the heart deprives cardiomyocytes of oxygen, triggering cell death (myocardial infarction). Ischemia and its cell culture model, hypoxia, elicit a stress response program that contributes to cardiomyocyte death; however, the molecular components required to promote this process remain nebulous. Gene 33 is a 50-kDa cytosolic adapter protein that suppresses signaling from receptor Tyr kinases of the epidermal growth factor receptor/ErbB family. Here we show that adenoviral expression of Gene 33 swiftly stimulates cardiomyocyte death coincident with reduced Akt and extracellular signal-regulated kinase (ERK) signaling. Subjecting cardiomyocytes to hypoxia and then reoxygenation induces gene 33 mRNA and Gene 33 protein. RNA interference experiments indicate that endogenous Gene 33 reduces Akt and ERK signaling and is required for maximal hypoxia-induced cardiomyocyte death. Gene 33 levels are also strikingly increased in myocardial ischemic injury and infarction. Our results identify a new role for Gene 33 as a component in the molecular pathophysiology of ischemic injury.
机译：心脏局部缺血会剥夺心肌细胞的氧气，引发细胞死亡（心肌梗塞）。缺血及其细胞培养模型（缺氧）会引发应激反应程序，从而导致心肌细胞死亡。但是，促进该过程所需的分子成分仍然模糊。基因33是一种50 kDa的胞质衔接蛋白，可抑制表皮生长因子受体/ ErbB家族的受体Tyr激酶发出的信号。在这里，我们显示基因33的腺病毒表达迅速刺激心肌细胞死亡，同时降低了Akt和细胞外信号调节激酶（ERK）信号传导。使心肌细胞缺氧，然后再充氧诱导 gene 33 mRNA和Gene 33蛋白。 RNA干扰实验表明，内源性基因33降低了Akt和ERK信号传导，是最大的缺氧诱导的心肌细胞死亡所必需的。心肌缺血性损伤和梗死中基因33水平也显着增加。我们的结果确定了基因33在缺血性损伤的分子病理生理中的新作用。

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