PTEN mediates serum deprivation-induced cytotoxicity in H9c2 cells via the PI3K/AKT signaling pathway
PTEN mediates serum deprivation-induced cytotoxicity in H9c2 cells via the PI3K/AKT signaling pathway
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PTEN 通过 PI3K/AKT 信号通路介导 H9c2 细胞中血清剥夺诱导的细胞毒性
DOI：
10.1016/j.tiv.2021.105131
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发表时间：
2021-03-15
影响因子：
3.2
通讯作者：
Wei, Yidong
中科院分区：
文献类型：
--
作者：
Gong, Mengmeng;Li, Zhiqiang;Wei, Yidong
急性心肌梗死（AMI）的发病机制与心肌细胞坏死和凋亡有关。许多研究已经确定了磷酸酶和张力蛋白同源物（PTEN）在其他细胞类型中的细胞增殖和凋亡的调节作用。然而，PTEN在心肌细胞中的潜在作用尚不清楚。在这项研究中，我们使用血清剥夺培养的H9 c2细胞来模拟心肌梗死的凋亡过程。用小干扰RNA（siRNA）敲低PTEN基因的表达。CCK-8法测定细胞活力。Edu染色检测细胞增殖，Western blot检测蛋白表达。我们还评估了ROS的产生，DNA损伤的程度，和细胞凋亡，用免疫荧光法。因此，我们观察到，在H9 c2细胞中的血清剥夺增加了PTEN的表达。在功能上，使用siRNA的PTEN敲除实验抑制血清剥夺诱导的细胞凋亡、ROS产生和DNA损伤，而增加细胞增殖。这些作用均可被磷脂酰肌醇3激酶（PI 3 K）抑制剂逆转，提示PI 3 K/蛋白激酶B（AKT）可能是血清缺乏时PTEN作用的关键成分。总之，我们的研究表明，PTEN/PI 3 K/AKT通路在血清剥夺诱导的H9 c2细胞毒性中的作用。
The pathogenesis of acute myocardial infarction (AMI) is associated with cardiomyocyte necrosis and apoptosis. Numerous studies have determined the regulatory effects of Phosphatase and tensin homolog (PTEN) cell proliferation and apoptosis in other cell types. However, the potential role of PTEN in cardiomyocyte is unclear. In this study, we used H9c2 cells cultured under serum deprivation to simulate the apoptosis process of myocardial infarction. Small interference RNA (siRNA) of PTEN was used to knock down the expression of PTEN. Cell viability was determined by CCK-8. Cell proliferation was examined by Edu staining, and the protein expression was analyzed by Western blot. We also evaluated the generation of ROS, the degree of DNA damage, and cell apoptosis using immunofluorescence assay. As a result, we observed that serum deprivation in H9c2 cells increased PTEN expression. Functionally, the PTEN knockdown experiment using siRNA inhibited serum deprivation-induced cell apoptosis, ROS production, and DNA damage, whereas increased cell proliferation. All these effects could be reversed by phosphatidylinositol 3-kinase (PI3K) inhibitor, which indicated the PI3K/ protein kinase B (AKT) might be the critical component of the PTEN effects during serum deficiency. In conclusion, our study indicated the role of the PTEN/PI3K/AKT pathway in serum deprivation-induced cytotoxicity in H9c2 cells.