c-Jun promotes the survival of H9c2 cells under hypoxia via PTEN/Akt signaling pathway

• Autores: Fan Wu, Feng Gao, Siyi He, Yunhan Jiang, Guiping Luo, Yingbin Xiao
• Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 75, Nº. 4, 2019, págs. 433-441
• Idioma: inglés
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• Resumen

  • 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.