Ischemia and hypoxia are common pathophysiological characteristics in cardiovascular diseases. c-Jun expression could be induced by extra- or intracellular stimuli and plays a pivotal role in regulating cell survival in response to the stress. However, previous studies of c-Jun in cell proliferation and apoptosis showed conflicting results. In the present study, we demonstrated that the expression of c-Jun was induced by hypoxia in H9c2 cells. Loss of function of c-Jun was investigated by CCK-8, LDH, and TUNEL assays in low oxygen (1% O₂) conditions. We revealed that c-Jun could promote cell survival and inhibit cell apoptosis under hypoxia. Knockdown of c-Jun also promoted the expression of apoptosis-related proteins under hypoxia, such as cleaved caspase-3, cleaved caspase-9, Bax, and Bim. Furthermore, we demonstrated that the knockdown of c-Jun inhibited the PTEN/Akt signaling pathway under hypoxia. Our findings suggested that c-Jun protected H9c2 cells from apoptosis and promoted the survival of H9c2 cells under hypoxia via PTEN/Akt signaling pathway.

中文翻译：

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c-Jun通过PTEN / Akt信号通路促进缺氧条件下H9c2细胞的存活。

缺血和缺氧是心血管疾病的常见病理生理特征。c-Jun表达可由细胞外或细胞内刺激诱导，并在调节细胞对应激的存活中起关键作用。但是，先前对c-Jun的细胞增殖和凋亡研究显示出矛盾的结果。在本研究中，我们证明了缺氧诱导H9c2细胞中c-Jun的表达。通过CCK-8，LDH和TUNEL分析在低氧（1％O ₂） 条件。我们发现c-Jun在缺氧条件下可以促进细胞存活并抑制细胞凋亡。敲低c-Jun还能促进缺氧条件下凋亡相关蛋白的表达，例如caspase-3裂解，caspase-9裂解，Bax和Bim裂解。此外，我们证明了敲低c-Jun可以抑制缺氧条件下的PTEN / Akt信号通路。我们的发现表明c-Jun通过PTEN / Akt信号通路保护H9c2细胞免于凋亡，并促进H9c2细胞在缺氧条件下的存活。