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Role of reactive oxygen species-MAP ...

Gurjar, Milind Vasudeo.

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Role of reactive oxygen species-MAP kinase signaling and nitric oxide in matrix metalloproteinase-9 induction in vascular smooth muscle cells.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Role of reactive oxygen species-MAP kinase signaling and nitric oxide in matrix metalloproteinase-9 induction in vascular smooth muscle cells./
Author:	Gurjar, Milind Vasudeo.
Description:	126 p.
Notes:	Source: Dissertation Abstracts International, Volume: 62-06, Section: B, page: 2561.
Contained By:	Dissertation Abstracts International62-06B.
Subject:	Biology, Anatomy. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3018579
ISBN:	0493298010

Role of reactive oxygen species-MAP kinase signaling and nitric oxide in matrix metalloproteinase-9 induction in vascular smooth muscle cells.
Gurjar, Milind Vasudeo.

Role of reactive oxygen species-MAP kinase signaling and nitric oxide in matrix metalloproteinase-9 induction in vascular smooth muscle cells. - 126 p.

Source: Dissertation Abstracts International, Volume: 62-06, Section: B, page: 2561.

Thesis (Ph.D.)--The University of Iowa, 2001.

Extracellular matrix breakdown is important for vascular smooth muscle cell migration and vascular remodeling, and requires matrix metalloproteinases. MMP-9 is an inducible enzyme, and is increased in atherosclerotic plaques and in balloon-injured arteries. IL-1β is a cytokine increased at the site of vascular injury, and stimulates MMP9 induction. The aim of the present study was to investigate the role of superoxide and extracellular-signal regulated kinase pathway in IL-1β-stimulated MMP-9 induction in vascular smooth muscle cells.

ISBN: 0493298010Subjects--Topical Terms:

1021727
Biology, Anatomy.

Role of reactive oxygen species-MAP kinase signaling and nitric oxide in matrix metalloproteinase-9 induction in vascular smooth muscle cells.
LDR:03559nam 2200313 a 45 001 927547
005 20110425
008 110425s2001 eng d
020 $a 0493298010
035 $a (UnM)AAI3018579
035 $a AAI3018579
040 $a UnM $c UnM
100 1 $a Gurjar, Milind Vasudeo. $3 1251108
245 1 0 $a Role of reactive oxygen species-MAP kinase signaling and nitric oxide in matrix metalloproteinase-9 induction in vascular smooth muscle cells.
300 $a 126 p.
500 $a Source: Dissertation Abstracts International, Volume: 62-06, Section: B, page: 2561.
500 $a Supervisor: Ramesh C. Bhalla.
502 $a Thesis (Ph.D.)--The University of Iowa, 2001.
520 $a Extracellular matrix breakdown is important for vascular smooth muscle cell migration and vascular remodeling, and requires matrix metalloproteinases. MMP-9 is an inducible enzyme, and is increased in atherosclerotic plaques and in balloon-injured arteries. IL-1β is a cytokine increased at the site of vascular injury, and stimulates MMP9 induction. The aim of the present study was to investigate the role of superoxide and extracellular-signal regulated kinase pathway in IL-1β-stimulated MMP-9 induction in vascular smooth muscle cells.
520 $a Superoxide generation using xanthine-xanthine oxidase system stimulated ERK-dependent MMP-9 induction. Stimulation of VSM cells with IL-1β resulted in superoxide production, sustained ERK activation, and MMP-9 induction. Overexpression of MnSOD gene and N-acetyl cysteine treatment attenuated IL-1β-stimulated superoxide production. Treatment of cells with NAC or overexpression of MnSOD gene to inhibit superoxide production resulted in inhibition of sustained ERK activation and MMP-9 induction. Inhibition of IL-1β-stimulated sustained ERK activation by a specific inhibitor PD 98059, also inhibited MMP-9 induction. These results suggest that IL-1β-stimulated superoxide production leads to sustained ERK activation, which in turn is required for MMP-9 induction in VSM cells. The present study for the first time suggests a role of superoxide in IL-1β-stimulated sustained ERK activation and MMP-9 induction.
520 $a Endothelial dysfunction or injury decreases nitric oxide production in the vessel wall. Superoxide reacts with nitric oxide with a high degree of affinity and is suggested to decrease nitric oxide bioactivity. I have demonstrated that nitric oxide generation by eNOS gene transfer or by pharmacological approaches inhibits VSM cell migration and IL-1β-stimulated MMP-9 induction. Treatment of cells with nitric oxide donor inhibited IL-β-stimulated superoxide production and sustained ERK activation. These results suggest that nitric oxide inhibits IL-1β-stimulated MMP-9 induction by inhibition of superoxide-ERK signaling. Since MMP-9 is involved in VSM cell migration and neointima formation, the present studies suggest possible mechanisms by which nitric oxide regulates these processes.
520 $a In conclusion, modulation of inflammatory responses by regulation of reactive oxygen species generation using either pharmacological approaches or gene therapy protocol provide possible therapeutic targets to control the progression of vasoproliferative diseases.
590 $a School code: 0096.
650 4 $a Biology, Anatomy. $3 1021727
650 4 $a Biology, Cell. $3 1017686
690 $a 0287
690 $a 0379
710 2 0 $a The University of Iowa. $3 1017439
773 0 $t Dissertation Abstracts International $g 62-06B.
790 $a 0096
790 1 0 $a Bhalla, Ramesh C., $e advisor
791 $a Ph.D.
792 $a 2001
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3018579