Expression pattern of E2F6 in physical and chemical hypoxia-induced apoptosis.
- Author:
Bo SHU
1
;
Wei-Wei YANG
;
Huang-Tian YANG
Author Information
1. Laboratory of Molecular Cardiology of Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine (SJTUSM) and Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), Shanghai 200025, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Cell Hypoxia;
Cell Line;
Cobalt;
pharmacology;
Deferoxamine;
pharmacology;
Down-Regulation;
E2F6 Transcription Factor;
metabolism;
Myocytes, Cardiac;
cytology;
metabolism;
Rats
- From:
Acta Physiologica Sinica
2008;60(1):1-10
- CountryChina
- Language:English
-
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. However, 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 (CoCl(2)) induced apoptosis in H9c2 cells. Physical hypoxia- and CoCl(2)-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 CoCl(2)-induced apoptosis in H9c2 cells. In addition, the apoptosis induced by DFO may share different pathways from that induced by physical hypoxia and CoCl(2).
