Angiotensin II induces c-fos expression in smooth muscle via transcriptional control.

Naftilan, Allen J.; Pratt, Richard E.; Eldridge, Carol S.; Lin, Hui-Feng; Dzau, Victor J.

doi:10.1161/01.hyp.13.6.706

Cited by 199 publications

(54 citation statements)

References 32 publications

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“…In the neointima of experimental vein grafts, the AT 1 receptor is expressed focally and the degree of intimal hyperplasia is reduced significantly by the treatment with the AT 1 receptor antagonist losartan (20). In vitro studies confirm that Ang II directly promotes the growth of VSMC and the migration of the VSMC from the media into the intima (21)(22)(23). In the hyperplastic intima and media of the placebo-treated dogs, our immunohistochemical studies showed that the proliferative procedure but not the apoptotic procedure was evident and that there was a marked increase in the amount of the Ang II and AT 1 receptors.…”

Section: Discussionmentioning

confidence: 91%

Effect of Chymase Inhibition on the Arteriovenous Fistula Stenosis in Dogs

Jin

Ueda²,

Takai³

et al. 2005

Journal of the American Society of Nephrology

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It was hypothesized that chymase may participate in hemodialysis vascular access dysfunction, as chymase has been known to be an effective enzyme in the conversion of angiotensin I (Ang I) to Ang II and in the latent TGF-␤1 to the active form. An arteriovenous (AV) fistula was created between the brachial artery and vein in dogs. In the AV anastomosis, when the walls of the venous and arterial sides were compared, the eccentric neointimal formation was most evident in the venous wall. Compared with the venous side downstream of the AV anastomosis, a severe neointimal hyperplasia was found in the venous side upstream of the AV anastomosis (intima/media, 153 ؎ 25%). The chymase-and TGF-␤-positive mast cells were markedly accumulated in the proliferous neointima and media. In association with the reduction of chymase expression, a marked decrease in Ang II-, AT 1 receptor-, and TGF-␤-positive areas was achieved by NK3201 (a chymase inhibitor) treatment, and the neointima formation (intima/media: region A, 53 ؎ 9%, P < 0.001; region B, 54 ؎ 14%, P < 0.001) was also significantly suppressed in this group. Although lisinopril treatment also provided some beneficial effects with regard to the prevention of neointimal formation, the degree was less than that seen with chymase inhibition. These findings indicate that mast cell-derived chymase plays an essential role in the pathogenesis of the AV fistula access failure and that chymase inhibition may be a therapeutic target for the treatment of hemodialysis vascular access dysfunction in clinic settings.

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Section: Discussionmentioning

confidence: 91%

Effect of Chymase Inhibition on the Arteriovenous Fistula Stenosis in Dogs

Jin

Ueda²,

Takai³

et al. 2005

Journal of the American Society of Nephrology

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“…Exposure of VSMCs to Ang II leads to a dose-dependent and rapid induction in the immediate early response genes encoding c-fos, c-jun, and early growth response 1 (Egr-1) (6)(7)(8). The signal transducers and activators of transcription STAT1 and STAT2 are also activated via tyrosine phosphorylation in response to Ang II (9).…”

Section: Introductionmentioning

confidence: 99%

Ets-1 is a critical regulator of Ang II-mediated vascular inflammation and remodeling

Zhan

Brown²,

Maynard³

et al. 2005

Journal of Clinical Investigation

195

205

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Ang II is a central mediator of vascular inflammation and remodeling. The transcription factor Ets-1 is rapidly induced in vascular smooth muscle and endothelial cells of the mouse thoracic aorta in response to systemic Ang II infusion. Arterial wall thickening, perivascular fibrosis, and cardiac hypertrophy are significantly diminished in Ets1 -/-mice compared with control mice in response to Ang II. The induction of 2 known targets of Ets-1, cyclin-dependent kinase inhibitor p21 CIP and plasminogen activator inhibitor-1 (PAI-1), by Ang II is markedly blunted in the aorta of Ets1 -/-mice compared with wild-type controls. Expression of p21 CIP in VSMCs leads to cellular hypertrophy, whereas expression of p21 CIP in endothelial cells is associated with cell cycle arrest, apoptosis, and endothelial dysfunction. PAI-1 promotes the development of perivascular fibrosis. We have identified monocyte chemoattractant protein-1 (MCP-1) as a novel target for Ets-1. Expression of MCP-1 is similarly reduced in Ets1 -/-mice compared with control mice in response to Ang II, which results in significantly diminished recruitment of T cells and macrophages to the vessel wall. In summary, our results support a critical role for Ets-1 as a transcriptional mediator of vascular inflammation and remodeling in response to Ang II.

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“…3 Angiotensin II (Ang II), the main effector peptide of the reninangiotensin system has long been known to play a major role in the regulation of BP and body fluid homeostasis. Moreover, Ang II has been reported to induce hyperplasia and/or hypertrophy in cultured aortic smooth muscle cells [4][5][6][7] in small resistance arteries 8 and in cardiomyocytes. 9 The tissue response to Ang II is mediated by specific receptors located on the cell surface.…”

Section: Introductionmentioning

confidence: 99%

The potential role of angiotensin II in the vasculature

Levy

1998

J Hum Hypertens

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Arterial hypertension is associated with marked changes in the structure of both resistance and large arteries. The renin-angiotensin system is largely involved in these alterations; chronic blockade of the renin-angiotensin system prevents and/or reverses most of the alterations of the vasculature in experimental and clinical hypertension. In this review we have analysed the differential role of AT 1 and AT 2 receptors in the response of the vessels to arterial hypertension. It emerges that the relative involvement of each receptor

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Angiotensin II induces c-fos expression in smooth muscle via transcriptional control.

Cited by 199 publications

References 32 publications

Effect of Chymase Inhibition on the Arteriovenous Fistula Stenosis in Dogs

Effect of Chymase Inhibition on the Arteriovenous Fistula Stenosis in Dogs

Ets-1 is a critical regulator of Ang II-mediated vascular inflammation and remodeling

The potential role of angiotensin II in the vasculature

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