Expression pattern of E2F6 in physical and chemical hypoxia-induced apoptosis / 生理学报
Acta Physiologica Sinica
;
(6): 1-10, 2008.
Article
in English
| WPRIM
| ID: wpr-316768
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).
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Cell Hypoxia
/
Down-Regulation
/
Cell Line
/
Cobalt
/
Apoptosis
/
Cell Biology
/
Myocytes, Cardiac
/
Deferoxamine
/
E2F6 Transcription Factor
Type of study:
Prognostic study
Limits:
Animals
Language:
English
Journal:
Acta Physiologica Sinica
Year:
2008
Type:
Article
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