Essential role of vascular endothelial growth factor in angiotensin II-induced vascular inflammation and remodeling

Qingwei Zhao

Research output: Contribution to journalArticle

133 Citations (Scopus)

Abstract

Angiotensin II (Ang II) upregulates vascular endothelial growth factor (VEGF) and activates vascular inflammation. However, the decisive role of VEGF in Ang II-induced vascular inflammation and remodeling has not been addressed. Ang II infusion to wild-type mice increased local expression of VEGF and its receptors in cells of aortic wall and plasma VEGF, and caused aortic inflammation (monocyte infiltration) and remodeling (wall thickening and fibrosis). Hypoxia-inducible factor-1alpha colocalized with VEGF-positive cell types. Blockade of VEGF by the soluble VEGF receptor 1 (sFlt-1) gene transfer attenuated the Ang II-induced inflammation and remodeling. The sFlt-1 gene transfer also inhibited the increased expression of VEGF and inflammatory factors such as monocyte chemoattractant protein-1. In contrast, sFlt-1 gene transfer did not affect Ang II-induced arterial hypertension and cardiac hypertrophy. VEGF is an essential mediator in Ang II-induced vascular inflammation and structural changes through its proinflammatory actions.
Original languageEnglish
Pages (from-to)264-270
JournalHypertension
Volume44
StatePublished - Jul 19 2004

Fingerprint

Angiotensin II
Vascular Endothelial Growth Factor A
Inflammation
Blood Vessels
Genes
Vascular Endothelial Growth Factor Receptor-1
Vascular Endothelial Growth Factor Receptor
Chemokine CCL2
Cardiomegaly
Vascular Remodeling
Cell Wall
Monocytes
Fibrosis
Up-Regulation
Hypertension

Cite this

Essential role of vascular endothelial growth factor in angiotensin II-induced vascular inflammation and remodeling. / Zhao, Qingwei.

In: Hypertension, Vol. 44, 19.07.2004, p. 264-270.

Research output: Contribution to journalArticle

@article{b69d2f4030494e96a25eb9916dfb5f0e,
title = "Essential role of vascular endothelial growth factor in angiotensin II-induced vascular inflammation and remodeling",
abstract = "Angiotensin II (Ang II) upregulates vascular endothelial growth factor (VEGF) and activates vascular inflammation. However, the decisive role of VEGF in Ang II-induced vascular inflammation and remodeling has not been addressed. Ang II infusion to wild-type mice increased local expression of VEGF and its receptors in cells of aortic wall and plasma VEGF, and caused aortic inflammation (monocyte infiltration) and remodeling (wall thickening and fibrosis). Hypoxia-inducible factor-1alpha colocalized with VEGF-positive cell types. Blockade of VEGF by the soluble VEGF receptor 1 (sFlt-1) gene transfer attenuated the Ang II-induced inflammation and remodeling. The sFlt-1 gene transfer also inhibited the increased expression of VEGF and inflammatory factors such as monocyte chemoattractant protein-1. In contrast, sFlt-1 gene transfer did not affect Ang II-induced arterial hypertension and cardiac hypertrophy. VEGF is an essential mediator in Ang II-induced vascular inflammation and structural changes through its proinflammatory actions.",
author = "Qingwei Zhao",
year = "2004",
month = "7",
day = "19",
language = "English",
volume = "44",
pages = "264--270",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",

}

TY - JOUR

T1 - Essential role of vascular endothelial growth factor in angiotensin II-induced vascular inflammation and remodeling

AU - Zhao, Qingwei

PY - 2004/7/19

Y1 - 2004/7/19

N2 - Angiotensin II (Ang II) upregulates vascular endothelial growth factor (VEGF) and activates vascular inflammation. However, the decisive role of VEGF in Ang II-induced vascular inflammation and remodeling has not been addressed. Ang II infusion to wild-type mice increased local expression of VEGF and its receptors in cells of aortic wall and plasma VEGF, and caused aortic inflammation (monocyte infiltration) and remodeling (wall thickening and fibrosis). Hypoxia-inducible factor-1alpha colocalized with VEGF-positive cell types. Blockade of VEGF by the soluble VEGF receptor 1 (sFlt-1) gene transfer attenuated the Ang II-induced inflammation and remodeling. The sFlt-1 gene transfer also inhibited the increased expression of VEGF and inflammatory factors such as monocyte chemoattractant protein-1. In contrast, sFlt-1 gene transfer did not affect Ang II-induced arterial hypertension and cardiac hypertrophy. VEGF is an essential mediator in Ang II-induced vascular inflammation and structural changes through its proinflammatory actions.

AB - Angiotensin II (Ang II) upregulates vascular endothelial growth factor (VEGF) and activates vascular inflammation. However, the decisive role of VEGF in Ang II-induced vascular inflammation and remodeling has not been addressed. Ang II infusion to wild-type mice increased local expression of VEGF and its receptors in cells of aortic wall and plasma VEGF, and caused aortic inflammation (monocyte infiltration) and remodeling (wall thickening and fibrosis). Hypoxia-inducible factor-1alpha colocalized with VEGF-positive cell types. Blockade of VEGF by the soluble VEGF receptor 1 (sFlt-1) gene transfer attenuated the Ang II-induced inflammation and remodeling. The sFlt-1 gene transfer also inhibited the increased expression of VEGF and inflammatory factors such as monocyte chemoattractant protein-1. In contrast, sFlt-1 gene transfer did not affect Ang II-induced arterial hypertension and cardiac hypertrophy. VEGF is an essential mediator in Ang II-induced vascular inflammation and structural changes through its proinflammatory actions.

M3 - Article

VL - 44

SP - 264

EP - 270

JO - Hypertension

JF - Hypertension

SN - 0194-911X

ER -