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

Qingwei Zhao, Minako Ishibashi, Hiasa Ken-Ichi, Chunyan Tan, Akira Takeshita, Kensuke Egashira

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-1α 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
Number of pages7
JournalHypertension
Volume44
Issue number3
DOIs
Publication statusPublished - Sep 1 2004

Fingerprint

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

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Essential role of vascular endothelial growth factor in angiotensin II-induced vascular inflammation and remodeling. / Zhao, Qingwei; Ishibashi, Minako; Ken-Ichi, Hiasa; Tan, Chunyan; Takeshita, Akira; Egashira, Kensuke.

In: Hypertension, Vol. 44, No. 3, 01.09.2004, p. 264-270.

Research output: Contribution to journalArticle

Zhao, Qingwei ; Ishibashi, Minako ; Ken-Ichi, Hiasa ; Tan, Chunyan ; Takeshita, Akira ; Egashira, Kensuke. / Essential role of vascular endothelial growth factor in angiotensin II-induced vascular inflammation and remodeling. In: Hypertension. 2004 ; Vol. 44, No. 3. pp. 264-270.
@article{778ed65073df47ce981599e13ee7f1ff,
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-1α 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 and Minako Ishibashi and Hiasa Ken-Ichi and Chunyan Tan and Akira Takeshita and Kensuke Egashira",
year = "2004",
month = "9",
day = "1",
doi = "10.1161/01.HYP.0000138688.78906.6b",
language = "English",
volume = "44",
pages = "264--270",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

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

AU - Zhao, Qingwei

AU - Ishibashi, Minako

AU - Ken-Ichi, Hiasa

AU - Tan, Chunyan

AU - Takeshita, Akira

AU - Egashira, Kensuke

PY - 2004/9/1

Y1 - 2004/9/1

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-1α 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-1α 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.

UR - http://www.scopus.com/inward/record.url?scp=4444238183&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4444238183&partnerID=8YFLogxK

U2 - 10.1161/01.HYP.0000138688.78906.6b

DO - 10.1161/01.HYP.0000138688.78906.6b

M3 - Article

C2 - 15262905

AN - SCOPUS:4444238183

VL - 44

SP - 264

EP - 270

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 3

ER -