Reduced angiogenesis and delay in wound healing in angiotensin II type 1a receptor-deficient mice

被引：46

作者：

Kurosaka, Maya ^{[1
,2
]}

Suzuki, Tatsunori ^{[1
]}

Hosono, Kanako ^{[1
]}

Kamata, Yuji ^{[1
,2
]}

Fukamizu, Akiyoshi ^{[3
]}

Kitasato, Hidero ^{[4
]}

Fujita, Yoshikuni ^{[2
]}

Majima, Masataka ^{[1
]}

机构：

[1] Kitasato Univ, Sch Med, Dept Pharmacol, Kanagawa 2288555, Japan

[2] Kitasato Univ, Sch Med, Dept Internal Med, Kanagawa 2288555, Japan

[3] Univ Tsukuba, Fac Sci, Dept Biol, Ibaraki, Japan

[4] Kitasato Univ, Sch Allied Hlth Sci, Dept Microbiol, Kanagawa 2288555, Japan

来源：

BIOMEDICINE & PHARMACOTHERAPY | 2009年 / 63卷 / 09期

关键词：

Angiogenesis; Angiotensin II; Wound healing; ENDOTHELIAL GROWTH-FACTOR; CONVERTING ENZYME; RETINAL PERICYTES; DEPENDENT PATHWAY; UP-REGULATION; TUMOR-GROWTH; EXPRESSION; CHYMASE; CELLS; GENE;

D O I：

10.1016/j.biopha.2009.01.001

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Angiotensin II (Ang II) is a bioactive peptide that plays important roles in blood pressure regulation and salt-water homeostasis. Recently, Ang II was reported to function in the promotion of angiogenesis. Since the wound healing process is highly dependent upon angiogenesis, we employed Ang II receptor knockout mice (AT1a(-/-)) to investigate whether or not Ang II facilitates angiogenesis and wound healing via AT1a receptor signaling. In comparison to wild-type (WT) mice, wound healing and wound-induced angiogenesis were significantly suppressed in AT1a(-/-) mice, and these mice exhibited reduced expression of CD31 in wound granulation tissues. In comparison to vehicle-treated mice, wound healing was delayed significantly in mice treated with an AT1-R antagonist and this delay was accompanied by the reduced expression of vascular endothelial growth factor in wound granulation tissues. These findings suggest that Ang II-AT1a signaling plays a crucial role in wound healing and wound-induced angiogenesis. (C) 2009 Elsevier Masson SAS. All rights reserved.

引用

页码：627 / 634

页数：8

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