Nox4 NADPH oxidase mediates peroxynitrite-dependent uncoupling of endothelial nitric-oxide synthase and fibronectin expression in response to angiotensin II: Role of mitochondrial reactive oxygen species

Doug Yoon Lee; Fabien Wauquier; Assaad A. Eid; Linda J. Roman; Goutam Ghosh-Choudhury; Khaled Khazim; Karen Block; Yves Gorin

doi:10.1074/jbc.M113.470971

Nox4 NADPH oxidase mediates peroxynitrite-dependent uncoupling of endothelial nitric-oxide synthase and fibronectin expression in response to angiotensin II: Role of mitochondrial reactive oxygen species

Doug Yoon Lee, Fabien Wauquier, Assaad A. Eid, Linda J. Roman, Goutam Ghosh-Choudhury, Khaled Khazim, Karen Block, Yves Gorin

Research output: Contribution to journal › Article › peer-review

108 Scopus citations

Abstract

Background:Oxidative stress is critical for the fibrotic response of mesangial cells (MCs) to angiotensin II. Results:Nox4- and mitochondrial reactive oxygen species (ROS)-dependent endothelial nitric-oxide synthase (eNOS) uncoupling led to fibronectin accumulation in MCs stimulated by angiotensin II. Conclusion:The Nox4/mitochondrial ROS/eNOS pathway mediates angiotensin II-induced MC injury. Significance:Targeting Nox4 and mitochondrial ROS is a promising therapeutic approach.

Original language	English (US)
Pages (from-to)	28668-28686
Number of pages	19
Journal	Journal of Biological Chemistry
Volume	288
Issue number	40
DOIs	https://doi.org/10.1074/jbc.M113.470971
State	Published - Oct 4 2013

ASJC Scopus subject areas

Molecular Biology
Biochemistry
Cell Biology

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Lee, D. Y., Wauquier, F., Eid, A. A., Roman, L. J., Ghosh-Choudhury, G., Khazim, K., Block, K., & Gorin, Y. (2013). Nox4 NADPH oxidase mediates peroxynitrite-dependent uncoupling of endothelial nitric-oxide synthase and fibronectin expression in response to angiotensin II: Role of mitochondrial reactive oxygen species. Journal of Biological Chemistry, 288(40), 28668-28686. https://doi.org/10.1074/jbc.M113.470971

Nox4 NADPH oxidase mediates peroxynitrite-dependent uncoupling of endothelial nitric-oxide synthase and fibronectin expression in response to angiotensin II: Role of mitochondrial reactive oxygen species. / Lee, Doug Yoon; Wauquier, Fabien; Eid, Assaad A. et al.
In: Journal of Biological Chemistry, Vol. 288, No. 40, 04.10.2013, p. 28668-28686.

Research output: Contribution to journal › Article › peer-review

Lee, DY, Wauquier, F, Eid, AA, Roman, LJ, Ghosh-Choudhury, G, Khazim, K, Block, K & Gorin, Y 2013, 'Nox4 NADPH oxidase mediates peroxynitrite-dependent uncoupling of endothelial nitric-oxide synthase and fibronectin expression in response to angiotensin II: Role of mitochondrial reactive oxygen species', Journal of Biological Chemistry, vol. 288, no. 40, pp. 28668-28686. https://doi.org/10.1074/jbc.M113.470971

Lee DY, Wauquier F, Eid AA, Roman LJ, Ghosh-Choudhury G, Khazim K et al. Nox4 NADPH oxidase mediates peroxynitrite-dependent uncoupling of endothelial nitric-oxide synthase and fibronectin expression in response to angiotensin II: Role of mitochondrial reactive oxygen species. Journal of Biological Chemistry. 2013 Oct 4;288(40):28668-28686. doi: 10.1074/jbc.M113.470971

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abstract = "Background:Oxidative stress is critical for the fibrotic response of mesangial cells (MCs) to angiotensin II. Results:Nox4- and mitochondrial reactive oxygen species (ROS)-dependent endothelial nitric-oxide synthase (eNOS) uncoupling led to fibronectin accumulation in MCs stimulated by angiotensin II. Conclusion:The Nox4/mitochondrial ROS/eNOS pathway mediates angiotensin II-induced MC injury. Significance:Targeting Nox4 and mitochondrial ROS is a promising therapeutic approach.",

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AU - Eid, Assaad A.

AU - Roman, Linda J.

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AU - Khazim, Khaled

AU - Block, Karen

AU - Gorin, Yves

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AB - Background:Oxidative stress is critical for the fibrotic response of mesangial cells (MCs) to angiotensin II. Results:Nox4- and mitochondrial reactive oxygen species (ROS)-dependent endothelial nitric-oxide synthase (eNOS) uncoupling led to fibronectin accumulation in MCs stimulated by angiotensin II. Conclusion:The Nox4/mitochondrial ROS/eNOS pathway mediates angiotensin II-induced MC injury. Significance:Targeting Nox4 and mitochondrial ROS is a promising therapeutic approach.

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Nox4 NADPH oxidase mediates peroxynitrite-dependent uncoupling of endothelial nitric-oxide synthase and fibronectin expression in response to angiotensin II: Role of mitochondrial reactive oxygen species

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