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Increased expression of Nox1 in neointimal smooth muscle cells promotes activation of matrix metalloproteinase-9

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Increased expression of Nox1 in neointimal smooth muscle cells promotes activation of matrix metalloproteinase-9. / Xu, Shaoping; Shriver, Amy S; Jagadeesha, Dammanahalli K; Chamseddine, Ali H; Szőcs, Katalin; Weintraub, Neal L; Griendling, Kathy K; Bhalla, Ramesh C; Miller, Francis J.

In: J VASC RES, Vol. 49, No. 3, 2012, p. 242-248.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Xu, S, Shriver, AS, Jagadeesha, DK, Chamseddine, AH, Szőcs, K, Weintraub, NL, Griendling, KK, Bhalla, RC & Miller, FJ 2012, 'Increased expression of Nox1 in neointimal smooth muscle cells promotes activation of matrix metalloproteinase-9', J VASC RES, vol. 49, no. 3, pp. 242-248. https://doi.org/10.1159/000332958

APA

Xu, S., Shriver, A. S., Jagadeesha, D. K., Chamseddine, A. H., Szőcs, K., Weintraub, N. L., Griendling, K. K., Bhalla, R. C., & Miller, F. J. (2012). Increased expression of Nox1 in neointimal smooth muscle cells promotes activation of matrix metalloproteinase-9. J VASC RES, 49(3), 242-248. https://doi.org/10.1159/000332958

Vancouver

Xu S, Shriver AS, Jagadeesha DK, Chamseddine AH, Szőcs K, Weintraub NL et al. Increased expression of Nox1 in neointimal smooth muscle cells promotes activation of matrix metalloproteinase-9. J VASC RES. 2012;49(3):242-248. https://doi.org/10.1159/000332958

Bibtex

@article{efe603e8d7eb4ada978a9cabf5ac1973,
title = "Increased expression of Nox1 in neointimal smooth muscle cells promotes activation of matrix metalloproteinase-9",
abstract = "OBJECTIVE: Vascular injury causes neointimal hypertrophy, which is characterized by redox-mediated matrix degradation and smooth muscle cell (SMC) migration and proliferation. We hypothesized that, as compared to the adjacent medial SMCs, neointimal SMCs produce increased superoxide via NADPH oxidase, which induces redox-sensitive intracellular signaling to activate matrix metalloproteinase-9 (MMP-9).METHODS AND RESULTS: Two weeks after balloon injury, rat aorta developed a prominent neointima, containing increased expression of NADPH oxidase and reactive oxygen species (ROS) as compared to the medial layer. Next, SMCs were isolated from either the neointima or the media and studied in culture. Neointimal-derived SMCs exhibited increased Nox1 expression and ROS levels as compared to medial SMCs. Neointimal SMCs had higher cell growth rates than medial SMCs. ROS-dependent ERK1/2 phosphorylation was greater in neointimal SMCs. MMP-9 activity, as detected by gel zymography, was greater in neointimal SMCs under resting and stimulated conditions and was prevented by expression of an antisense to Nox1 or treatment with an ERK1/2 inhibitor.CONCLUSIONS: Following vascular injury, the increased expression of Nox1 in SMCs within the neointima initiates redox-dependent phosphorylation of ERK1/2 and subsequent MMP-9 activation.",
keywords = "Animals, Cells, Cultured, Enzyme Activation, Extracellular Signal-Regulated MAP Kinases/metabolism, Matrix Metalloproteinase 9/metabolism, Muscle, Smooth, Vascular/cytology, Myocytes, Smooth Muscle/metabolism, NADH, NADPH Oxidoreductases/physiology, NADPH Oxidase 1, Neointima/metabolism, Rats, Reactive Oxygen Species/metabolism, Superoxide Dismutase/metabolism",
author = "Shaoping Xu and Shriver, {Amy S} and Jagadeesha, {Dammanahalli K} and Chamseddine, {Ali H} and Katalin Sz{\H o}cs and Weintraub, {Neal L} and Griendling, {Kathy K} and Bhalla, {Ramesh C} and Miller, {Francis J}",
note = "Copyright {\textcopyright} 2012 S. Karger AG, Basel.",
year = "2012",
doi = "10.1159/000332958",
language = "English",
volume = "49",
pages = "242--248",
number = "3",

}

RIS

TY - JOUR

T1 - Increased expression of Nox1 in neointimal smooth muscle cells promotes activation of matrix metalloproteinase-9

AU - Xu, Shaoping

AU - Shriver, Amy S

AU - Jagadeesha, Dammanahalli K

AU - Chamseddine, Ali H

AU - Szőcs, Katalin

AU - Weintraub, Neal L

AU - Griendling, Kathy K

AU - Bhalla, Ramesh C

AU - Miller, Francis J

N1 - Copyright © 2012 S. Karger AG, Basel.

PY - 2012

Y1 - 2012

N2 - OBJECTIVE: Vascular injury causes neointimal hypertrophy, which is characterized by redox-mediated matrix degradation and smooth muscle cell (SMC) migration and proliferation. We hypothesized that, as compared to the adjacent medial SMCs, neointimal SMCs produce increased superoxide via NADPH oxidase, which induces redox-sensitive intracellular signaling to activate matrix metalloproteinase-9 (MMP-9).METHODS AND RESULTS: Two weeks after balloon injury, rat aorta developed a prominent neointima, containing increased expression of NADPH oxidase and reactive oxygen species (ROS) as compared to the medial layer. Next, SMCs were isolated from either the neointima or the media and studied in culture. Neointimal-derived SMCs exhibited increased Nox1 expression and ROS levels as compared to medial SMCs. Neointimal SMCs had higher cell growth rates than medial SMCs. ROS-dependent ERK1/2 phosphorylation was greater in neointimal SMCs. MMP-9 activity, as detected by gel zymography, was greater in neointimal SMCs under resting and stimulated conditions and was prevented by expression of an antisense to Nox1 or treatment with an ERK1/2 inhibitor.CONCLUSIONS: Following vascular injury, the increased expression of Nox1 in SMCs within the neointima initiates redox-dependent phosphorylation of ERK1/2 and subsequent MMP-9 activation.

AB - OBJECTIVE: Vascular injury causes neointimal hypertrophy, which is characterized by redox-mediated matrix degradation and smooth muscle cell (SMC) migration and proliferation. We hypothesized that, as compared to the adjacent medial SMCs, neointimal SMCs produce increased superoxide via NADPH oxidase, which induces redox-sensitive intracellular signaling to activate matrix metalloproteinase-9 (MMP-9).METHODS AND RESULTS: Two weeks after balloon injury, rat aorta developed a prominent neointima, containing increased expression of NADPH oxidase and reactive oxygen species (ROS) as compared to the medial layer. Next, SMCs were isolated from either the neointima or the media and studied in culture. Neointimal-derived SMCs exhibited increased Nox1 expression and ROS levels as compared to medial SMCs. Neointimal SMCs had higher cell growth rates than medial SMCs. ROS-dependent ERK1/2 phosphorylation was greater in neointimal SMCs. MMP-9 activity, as detected by gel zymography, was greater in neointimal SMCs under resting and stimulated conditions and was prevented by expression of an antisense to Nox1 or treatment with an ERK1/2 inhibitor.CONCLUSIONS: Following vascular injury, the increased expression of Nox1 in SMCs within the neointima initiates redox-dependent phosphorylation of ERK1/2 and subsequent MMP-9 activation.

KW - Animals

KW - Cells, Cultured

KW - Enzyme Activation

KW - Extracellular Signal-Regulated MAP Kinases/metabolism

KW - Matrix Metalloproteinase 9/metabolism

KW - Muscle, Smooth, Vascular/cytology

KW - Myocytes, Smooth Muscle/metabolism

KW - NADH, NADPH Oxidoreductases/physiology

KW - NADPH Oxidase 1

KW - Neointima/metabolism

KW - Rats

KW - Reactive Oxygen Species/metabolism

KW - Superoxide Dismutase/metabolism

U2 - 10.1159/000332958

DO - 10.1159/000332958

M3 - SCORING: Journal article

C2 - 22433789

VL - 49

SP - 242

EP - 248

IS - 3

ER -