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.
Keywords: Apoptosis; Cardiomyocytes; H9c2 cells; Hypoxia; c-Jun.