Department of Cardiovascular Surgery, General Hospital of Western Theater Command, Chengdu, 610083, Sichuan, People's Republic of China.
Department of Cardiovascular Surgery, Xinqiao Hospital, Army Medical University, Xinqiao Street, Shapingba District, Chongqing, 400037, People's Republic of China.
J Physiol Biochem. 2019 Nov;75(4):433-441. doi: 10.1007/s13105-019-00695-3. Epub 2019 Aug 3.
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% O) 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.
缺血和缺氧是心血管疾病中常见的病理生理特征。c-Jun 的表达可被细胞外或细胞内刺激诱导，在调节细胞对应激的存活中发挥关键作用。然而，之前关于 c-Jun 在细胞增殖和凋亡中的研究结果存在矛盾。在本研究中，我们证明了 c-Jun 在 H9c2 细胞中由缺氧诱导表达。在低氧（1% O）条件下，通过 CCK-8、LDH 和 TUNEL 测定法研究了 c-Jun 的功能丧失。我们揭示 c-Jun 可以促进缺氧条件下的细胞存活并抑制细胞凋亡。c-Jun 的敲低也促进了缺氧下凋亡相关蛋白的表达，如 cleaved caspase-3、cleaved caspase-9、Bax 和 Bim。此外，我们证明了 c-Jun 的敲低抑制了缺氧下的 PTEN/Akt 信号通路。我们的研究结果表明，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。
