Abstract:
Apoptosis can be caused by hypoxia,a major factor during ischemic injury,in cardiomyocytes.However,the regulatory mechanisms underlying hypoxia-induced cardiomyocyte apoptosis have not yet been fully understood.E2F6,an identified E2F family member,has been demonstrated to repress DNA damage-induced apoptosis in our recent study.HoweveL it is unclear whether E2F6 is involved in hypoxia-induced apoptosis.In this study,we determined the expression property of E2F6 during hypoxia-induced apoptosis in H9c2 cells,a rat ventricular myoblast cell line.The results showed that physical hypoxia and chemical hypoxia-mimetic agents desferrioxamine(DFO)and cobalt chloride(CoCl2)induced apoptosis in H9c2 cells.Physical hypoxia-and CoCl2-induced apoptosis was accompanied with a downregulation of endogenous E2F6 mRNA expression,but not protein expression.DFO treatment resulted in a significant downregulation of both mRNA and protein expressions of endogenous E2F6.These results suggest that E2F6 may be involved in DFO-induced apoptosis,while it is less sensitive in physical hypoxia-and CoCl2-induced apoptosis in H9c2 cells.In addition,the apoptosis induced by DFO may share different pathways from that induced by physical hypoxia and CoCl2.