STAT1 (signal transducer and activator of transcription 1) is potentially involved in cell survival, as well as cell death, in different types of cells. The present study was designed to examine the effects of STAT1 on hypoxia/re-oxygenation (H/R)-induced cell death and/or survival, and the underlying mechanisms of any such effects. H/R was shown to induce apoptotic cell death of rat hepatocytes. The addition of a STAT1-specific inhibitor, fludarabine, significantly increased the fraction of apoptotic cells after H/R. Following H/R, STAT1 was activated and sequential phosphorylation of Tyr701 and Ser727 was observed, which could be inhibited by the antioxidant N-acetyl-l-cysteine. Tyrosine and serine phosphorylation of STAT1 was mediated by Janus kinase 2 and phosphoinositide 3-kinase/Akt kinase respectively in a redox-dependent manner following H/R. STAT1-induced HSP70 (heat-shock protein 70) expression and the suppression of apoptosis occurred concomitantly. In conclusion, STAT1 activation, in a redox-dependent manner, following H/R may play crucial roles in cell survival, at least partly via HSP70 induction.
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Research Article|
May 15 2004
Hypoxia/re-oxygenation-induced, redox-dependent activation of STAT1 (signal transducer and activator of transcription 1) confers resistance to apoptotic cell death via hsp70 induction
Keita TERUI;
Keita TERUI
*Bioengineering Laboratory, Department of Innovative Surgery National Research Institute for Child Health and Development 3-35-31, Taishi-do, Setagaya, Tokyo, 154-8567, Japan
†Department of Pediatric Surgery, Chiba University Graduate School of Medicine, 1-8-1, Inohana, Chuo-ku, Chiba, 260-8677, Japan
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Sanae HAGA;
Sanae HAGA
*Bioengineering Laboratory, Department of Innovative Surgery National Research Institute for Child Health and Development 3-35-31, Taishi-do, Setagaya, Tokyo, 154-8567, Japan
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Shin ENOSAWA;
Shin ENOSAWA
*Bioengineering Laboratory, Department of Innovative Surgery National Research Institute for Child Health and Development 3-35-31, Taishi-do, Setagaya, Tokyo, 154-8567, Japan
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Naomi OHNUMA;
Naomi OHNUMA
†Department of Pediatric Surgery, Chiba University Graduate School of Medicine, 1-8-1, Inohana, Chuo-ku, Chiba, 260-8677, Japan
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Michitaka OZAKI
Michitaka OZAKI
1
*Bioengineering Laboratory, Department of Innovative Surgery National Research Institute for Child Health and Development 3-35-31, Taishi-do, Setagaya, Tokyo, 154-8567, Japan
‡Department of Food and Health Science, Okayama University Graduate School of Medicine and Dentistry, Faculty of Medicine, 2-5-1, Shikata-cho, Okayama, 700-8558, Japan
1To whom correspondence should be addressed (e-mail [email protected]).
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Publisher: Portland Press Ltd
Received:
December 08 2003
Revision Received:
February 24 2004
Accepted:
February 25 2004
Accepted Manuscript online:
February 25 2004
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London ©2004
2004
Biochem J (2004) 380 (1): 203–209.
Article history
Received:
December 08 2003
Revision Received:
February 24 2004
Accepted:
February 25 2004
Accepted Manuscript online:
February 25 2004
Citation
Keita TERUI, Sanae HAGA, Shin ENOSAWA, Naomi OHNUMA, Michitaka OZAKI; Hypoxia/re-oxygenation-induced, redox-dependent activation of STAT1 (signal transducer and activator of transcription 1) confers resistance to apoptotic cell death via hsp70 induction. Biochem J 15 May 2004; 380 (1): 203–209. doi: https://doi.org/10.1042/bj20031891
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