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STAT3 deletion sensitizes cells to oxidative stress

STAT3 deletion sensitizes cells to oxidative stress
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 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
STAT1, STAT3, apoptosis, ischemia, myocardial infarction, oxidative stress
0006-291X
324-329
Barry, Seán P.
be2c2533-9d53-4421-8acc-18c078e18452
Townsend, Paul A.
a2680443-664e-46d0-b4dd-97456ba810db
McCormick, James
9f5d47a6-87d4-48c3-a952-4133b710bbb1
Knight, Richard A.
da6172f8-cacc-4330-871a-85dea9e893a4
Scarabelli, Tiziano M.
ac96a777-880e-4e39-9884-f11a0978da35
Latchman, David S.
71e9db7c-9075-4b49-afac-6413085378db
Stephanou, Anastasis
e9d502e8-693c-4458-a3c6-5e2844665db3
Barry, Seán P.
be2c2533-9d53-4421-8acc-18c078e18452
Townsend, Paul A.
a2680443-664e-46d0-b4dd-97456ba810db
McCormick, James
9f5d47a6-87d4-48c3-a952-4133b710bbb1
Knight, Richard A.
da6172f8-cacc-4330-871a-85dea9e893a4
Scarabelli, Tiziano M.
ac96a777-880e-4e39-9884-f11a0978da35
Latchman, David S.
71e9db7c-9075-4b49-afac-6413085378db
Stephanou, Anastasis
e9d502e8-693c-4458-a3c6-5e2844665db3

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).

Record type: Article

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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More information

Published date: July 2009
Keywords: STAT1, STAT3, apoptosis, ischemia, myocardial infarction, oxidative stress

Identifiers

Local EPrints ID: 69513
URI: https://eprints.soton.ac.uk/id/eprint/69513
ISSN: 0006-291X
PURE UUID: dc8de5de-8b35-4257-9ea6-963c0cef676e

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Date deposited: 19 Nov 2009
Last modified: 19 Jul 2017 00:12

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Contributors

Author: Seán P. Barry
Author: Paul A. Townsend
Author: James McCormick
Author: Richard A. Knight
Author: Tiziano M. Scarabelli
Author: David S. Latchman
Author: Anastasis Stephanou

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