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Biomedicine and pharmacotherapy
Volume 63, n° 9
pages 627-634 (novembre 2009)
Doi : 10.1016/j.biopha.2009.01.001
Received : 17 November 2008 ;  accepted : 14 January 2009
Reduced angiogenesis and delay in wound healing in angiotensin II type 1a receptor-deficient mice

Maya Kurosaka a, b, Tatsunori Suzuki a, Kanako Hosono a, Yuji Kamata a, b, Akiyoshi Fukamizu c, Hidero Kitasato d, Yoshikuni Fujita b, Masataka Majima a,
a Department of Pharmacology, Kitasato University School of Medicine, Kanagawa, Japan 
b Department of Internal Medicine, Kitasato University School of Medicine, Kanagawa, Japan 
c Department of Biology, Faculty of Science Tsukuba University, Ibaraki, Japan 
d Department of Microbiology, Kitasato University School of Allied Health Science, Kanagawa, Japan 

Corresponding author. Department of Molecular Pharmacology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Sagamihara 228-8555, Kanagawa, Japan. Tel.: +81 42 778 8822; fax: +81 42 778 7604.

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.

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Keywords : Angiogenesis, Angiotensin II, Wound healing

© 2009  Elsevier Masson SAS. All Rights Reserved.