STAT3 deletion sensitizes cells to oxidative stress

被引：71

作者：

Barry, Sean P. ^{[1
]}

Townsend, Paul A. ^{[2
]}

McCormick, James ^{[1
]}

Knight, Richard A. ^{[1
]}

Scarabelli, Tiziano M. ^{[3
,4
]}

Latchman, David S. ^{[1
]}

Stephanou, Anastasis ^{[1
]}

机构：

[1] UCL, Inst Child Hlth, Med Mol Biol Unit, London WC1N 1EH, England

[2] Univ Southampton, Southampton Gen Hosp, Sch Med, Div Human Genet, Southampton, Hants, England

[3] Wayne State Univ, Sch Med, Ctr Heart & Vessel Preclin Studies, St John Hosp, Detroit, MI USA

[4] Wayne State Univ, Med Ctr, Sch Med, Detroit, MI 48202 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 385卷 / 03期

关键词：

STAT1; STAT3; Apoptosis; Ischemia; Myocardial infarction; Oxidative stress; SIGNAL TRANSDUCER; CARDIAC MYOCYTES; MOLECULAR TARGETS; TRANSCRIPTION-3; ACTIVATION; APOPTOSIS; GENE; ISCHEMIA/REPERFUSION; EXPRESSION; ISCHEMIA;

D O I：

10.1016/j.bbrc.2009.05.051

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

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. (C) 2009 Elsevier Inc. All rights reserved.

引用

页码：324 / 329

页数：6

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