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Biochem Biophys Res Commun. 2009 Jul 31;385(3):324-9. doi: 10.1016/j.bbrc.2009.05.051. Epub 2009 May 18.

STAT3 deletion sensitizes cells to oxidative stress.

Author information

1
Medical Molecular Biology Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N1EH, UK.

Abstract

The transcription factor STAT1 plays a role in promoting apoptotic cell death, whereas the related STAT3 transcription factor protects cardiac myocytes from ischemia/reperfusion (I/R) injury or oxidative stress. Cytokines belonging to the IL-6 family activate the JAK-STAT3 pathway, but also activate other cytoprotective pathways such as the MAPK-ERK or the PI3-AKT pathway. It is therefore unclear whether STAT3 is the only cytoprotective mediator against oxidative stress-induced cell death. Overexpression of STAT3 in primary neonatal rat ventricular myocytes (NRVM) protects against I/R-induced cell death. Moreover, a dominant negative STAT3 adenovirus (Ad ST3-DN) enhanced apoptotic cell death (81.2+/-6.9%) compared to control infected NRVM (46.0+/-3.1%) following I/R. Depletion of STAT3 sensitized cells to apoptotic cell death following oxidative stress. These results provide direct evidence for the role of STAT3 as a cytoprotective transcription factor in cells exposed to oxidative stress.

PMID:
19450559
PMCID:
PMC2706948
DOI:
10.1016/j.bbrc.2009.05.051
[Indexed for MEDLINE]
Free PMC Article

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