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 journalArticle

74 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)28668-28686
Number of pages19
JournalJournal of Biological Chemistry
Volume288
Issue number40
DOIs
StatePublished - Oct 4 2013

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Peroxynitrous Acid
Mesangial Cells
Nitric Oxide Synthase Type III
NADPH Oxidase
Fibronectins
Angiotensin II
Reactive Oxygen Species
Oxidative stress
Oxidative Stress
Wounds and Injuries
Therapeutics

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

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.; Roman, Linda J.; Ghosh-choudhury, Goutam; Khazim, Khaled; Block, Karen; Gorin, Yves.

In: Journal of Biological Chemistry, Vol. 288, No. 40, 04.10.2013, p. 28668-28686.

Research output: Contribution to journalArticle

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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 - Lee, Doug Yoon

AU - Wauquier, Fabien

AU - Eid, Assaad A.

AU - Roman, Linda J.

AU - Ghosh-choudhury, Goutam

AU - Khazim, Khaled

AU - Block, Karen

AU - Gorin, Yves

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Y1 - 2013/10/4

N2 - 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.

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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