STAT3 deletion sensitizes cells to oxidative stress

Barry, Seán P., Townsend, Paul A., McCormick, James, Knight, Richard A., Scarabelli, Tiziano M., Latchman, David S. and Stephanou, Anastasis (2009) STAT3 deletion sensitizes cells to oxidative stress. Biochemical and Biophysical Research Communications, 385 (3), 324-329. (doi:10.1016/j.bbrc.2009.05.051).

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

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