STAT3 deletion sensitizes cells to oxidative stress

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...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2009-07, Vol.385 (3), p.324-329
Main Authors: Barry, Seán P., Townsend, Paul A., McCormick, James, Knight, Richard A., Scarabelli, Tiziano M., Latchman, David S., Stephanou, Anastasis
Format: Article
Language:English
Subjects:
Adenovirus
Animals
Apoptosis
Apoptosis - genetics
Cell Line
Gene Deletion
Ischemia
Mice
Mutation
Myocardial infarction
Myocardial Reperfusion Injury - genetics
Myocytes, Cardiac - metabolism
Oxidative stress
Oxidative Stress - genetics
Rats
STAT1
STAT3
STAT3 Transcription Factor - deficiency
STAT3 Transcription Factor - genetics
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Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.05.051