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Cited by 839Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative Mechanisms

Novel gp91 phox Homologues in Vascular Smooth Muscle Cells: nox1 Mediates Angiotensin II–Induced Superoxide Formation and Redox-Sensitive Signaling Pathways

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Lassègue, Bernard, Sorescu, Dan, Szöcs, Katalin, Yin, QiQin, Akers, Marjorie, Zhang, Yong, Grant, Sharon L., Lambeth, J. David +1 more·2001·Circulation Research
DOI 10.1161/hh0901.090299
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Abstract

Abstract —Emerging evidence indicates that reactive oxygen species are important regulators of vascular function. Although NAD(P)H oxidases have been implicated as major sources of superoxide in the vessel wall, the molecular identity of these proteins remains unclear. We recently cloned nox1 (formerly mox-1), a member of a new family of gp91 phox homologues, and showed that it is expressed in proliferating vascular smooth muscle cells (VSMCs). In this study, we examined the expression of three nox family members, nox1, nox4, and gp91 phox , in VSMCs, their regulation by angiotensin II (Ang II), and their role in redox-sensitive signaling. We found that both nox1 and nox4 are expressed to a much higher degree than gp91 phox in VSMCs. Although serum, platelet-derived growth factor (PDGF), and Ang II downregulated nox4, they markedly upregulated nox1, suggesting that this enzyme may account for the delayed phase of superoxide production in these cells. Furthermore, an adenovirus expressing antisense nox1 mRNA completely inhibited the early phase of superoxide production induced by Ang II or PDGF and significantly decreased activation of the redox-sensitive signaling molecules p38 mitogen-activated protein kinase and Akt by Ang II. In contrast, redox-independent pathways induced by PDGF or Ang II were unaffected. These data support a role for nox1 in redox signaling in VSMCs and provide insight into the molecular identity of the VSMC NAD(P)H oxidase and its potentially critical role in vascular disease.

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  1. Ushio-Fukai M, Alexander RW, Akers M, Griendling KK. p38MAP kinase is a critical component of the redox-sensitive signaling pathways by angiotensin II: role in vascular smooth muscle cell hypertrophy. J Biol Chem. 1998;273:15022-15029.
  2. Zafari AM, Ushio-Fukai M, Akers M, Yin Q, Shah A, Harrison DG, Taylor WR, Griendling KK. Novel role of NADH/NADPH oxidase- derived hydrogen peroxide in angiotensin II-induced hypertrophy of rat vascular smooth muscle cells. Hypertension. 1998;32:488 -495.

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Authors
Lassègue, B., Sorescu, D., Szöcs, K., Yin, Q., Akers, M., Zhang, Y., Grant, S. L., Lambeth, J. D., & Griendling, K. K.
Affiliations
  • From the Department of Medicine, Division of Cardiology (B.L., D.S., K.S., Q.Q.Y., M.A., Y.Z., S.L.G., K.K.G.) and Department of Biochemistry (J.D.L.), Emory University, Atlanta, Ga.
  • Emory University (US)
ORCID
Venue
Circulation Research
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2001-05-11
Volume
88
Issue
9
Pages
888-894
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
DOI
10.1161/hh0901.090299
OpenAlex
W2145898095
Cited by
839
References
42
Citations by year
2026: 3 · 2025: 7 · 2024: 6 · 2023: 17 · 2022: 6 · 2021: 15 · 2020: 15 · 2019: 25 · 2018: 13 · 2017: 23 · 2016: 29 · 2015: 35 · 2014: 32 · 2013: 41 · 2012: 45
FWCI
33.66
Type
journal article
Language
en
Open access
Locations
  • Circulation Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Heart Association
  • Johns Hopkins University
  • Morehouse School of Medicine
  • National Institutes of Health
  • Centers for Disease Control and Prevention
  • National Heart, Lung, and Blood Institute (HL 58000, HL38206, HL58863, P01HL058000, R01HL058863)
  • National Cancer Institute (CA-84138, R01CA084138)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords
NOX1, NOX4, gp91phox, NADPH oxidase, vascular smooth muscle cells, reactive oxygen species, superoxide production, angiotensin II, platelet-derived growth factor, redox signaling, p38 MAPK, Akt, vascular disease
MeSH terms
NADPH Oxidase 1, NADPH Oxidase 2, NADPH Oxidase 4, Animals, Cell Line, Cells, Cultured, Dose-Response Relationship, Drug, Enzyme Inhibitors, Gene Expression Regulation, Indoles, Maleimides, Membrane Glycoproteins, Molecular Sequence Data, Muscle, Smooth, Vascular, NADH, NADPH Oxidoreductases, Oxidation-Reduction, Platelet-Derived Growth Factor, Protein Kinase C, RNA, Messenger, Superoxides, Time Factors, Blotting, Northern, Signal Transduction, Gene Expression, DNA, Antisense, Sequence Analysis, DNA, DNA, Complementary, NADPH Oxidases, Rats

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