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Novel gp91(phox) homologues in vascular smooth muscle cells: nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways

Standard

Novel gp91(phox) homologues in vascular smooth muscle cells: nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways. / Lassègue, B; Sorescu, D; Szöcs, K; Yin, Q; Akers, M; Zhang, Y; Grant, S L; Lambeth, J D; Griendling, K K.

in: CIRC RES, Jahrgang 88, Nr. 9, 11.05.2001, S. 888-894.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Lassègue, B, Sorescu, D, Szöcs, K, Yin, Q, Akers, M, Zhang, Y, Grant, SL, Lambeth, JD & Griendling, KK 2001, 'Novel gp91(phox) homologues in vascular smooth muscle cells: nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways', CIRC RES, Jg. 88, Nr. 9, S. 888-894. https://doi.org/10.1161/hh0901.090299

APA

Lassègue, B., Sorescu, D., Szöcs, K., Yin, Q., Akers, M., Zhang, Y., Grant, S. L., Lambeth, J. D., & Griendling, K. K. (2001). Novel gp91(phox) homologues in vascular smooth muscle cells: nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways. CIRC RES, 88(9), 888-894. https://doi.org/10.1161/hh0901.090299

Vancouver

Lassègue B, Sorescu D, Szöcs K, Yin Q, Akers M, Zhang Y et al. Novel gp91(phox) homologues in vascular smooth muscle cells: nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways. CIRC RES. 2001 Mai 11;88(9):888-894. https://doi.org/10.1161/hh0901.090299

Bibtex

@article{8d9ee366f7c64b8d9e1af46e559d88ec,
title = "Novel gp91(phox) homologues in vascular smooth muscle cells: nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways",
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.",
keywords = "Animals, Blotting, Northern, Cell Line, Cells, Cultured, DNA, Antisense/genetics, DNA, Complementary/chemistry, Dose-Response Relationship, Drug, Enzyme Inhibitors/pharmacology, Gene Expression, Gene Expression Regulation/drug effects, Indoles/pharmacology, Maleimides/pharmacology, Membrane Glycoproteins/genetics, Molecular Sequence Data, Muscle, Smooth, Vascular/cytology, NADH, NADPH Oxidoreductases/genetics, NADPH Oxidase 1, NADPH Oxidase 2, NADPH Oxidase 4, NADPH Oxidases/genetics, Oxidation-Reduction, Platelet-Derived Growth Factor/pharmacology, Protein Kinase C/antagonists & inhibitors, RNA, Messenger/drug effects, Rats, Sequence Analysis, DNA, Signal Transduction, Superoxides/metabolism, Time Factors",
author = "B Lass{\`e}gue and D Sorescu and K Sz{\"o}cs and Q Yin and M Akers and Y Zhang and Grant, {S L} and Lambeth, {J D} and Griendling, {K K}",
year = "2001",
month = may,
day = "11",
doi = "10.1161/hh0901.090299",
language = "English",
volume = "88",
pages = "888--894",
journal = "CIRC RES",
issn = "0009-7330",
publisher = "Lippincott Williams and Wilkins",
number = "9",

}

RIS

TY - JOUR

T1 - Novel gp91(phox) homologues in vascular smooth muscle cells: nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways

AU - Lassègue, B

AU - Sorescu, D

AU - Szöcs, K

AU - Yin, Q

AU - Akers, M

AU - Zhang, Y

AU - Grant, S L

AU - Lambeth, J D

AU - Griendling, K K

PY - 2001/5/11

Y1 - 2001/5/11

N2 - 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.

AB - 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.

KW - Animals

KW - Blotting, Northern

KW - Cell Line

KW - Cells, Cultured

KW - DNA, Antisense/genetics

KW - DNA, Complementary/chemistry

KW - Dose-Response Relationship, Drug

KW - Enzyme Inhibitors/pharmacology

KW - Gene Expression

KW - Gene Expression Regulation/drug effects

KW - Indoles/pharmacology

KW - Maleimides/pharmacology

KW - Membrane Glycoproteins/genetics

KW - Molecular Sequence Data

KW - Muscle, Smooth, Vascular/cytology

KW - NADH, NADPH Oxidoreductases/genetics

KW - NADPH Oxidase 1

KW - NADPH Oxidase 2

KW - NADPH Oxidase 4

KW - NADPH Oxidases/genetics

KW - Oxidation-Reduction

KW - Platelet-Derived Growth Factor/pharmacology

KW - Protein Kinase C/antagonists & inhibitors

KW - RNA, Messenger/drug effects

KW - Rats

KW - Sequence Analysis, DNA

KW - Signal Transduction

KW - Superoxides/metabolism

KW - Time Factors

U2 - 10.1161/hh0901.090299

DO - 10.1161/hh0901.090299

M3 - SCORING: Journal article

C2 - 11348997

VL - 88

SP - 888

EP - 894

JO - CIRC RES

JF - CIRC RES

SN - 0009-7330

IS - 9

ER -