Reduced angiogenesis and delay in wound healing in angiotensin II type 1a receptor-deficient mice.
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.
Kurosaka
Maya
M
Department of Pharmacology, Kitasato University School of Medicine, Kanagawa, Japan.
Suzuki
Tatsunori
T
Hosono
Kanako
K
Kamata
Yuji
Y
Fukamizu
Akiyoshi
A
Kitasato
Hidero
H
Fujita
Yoshikuni
Y
Majima
Masataka
M
D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018919:Neovascularization, Physiologic; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D044140:Receptor, Angiotensin, Type 1 / Q000032:analysis / Q000502:physiology*; D015398:Signal Transduction; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis / Q000502:physiology; D014945:Wound Healing
D047228:Angiotensin II Type 1 Receptor Blockers; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D044140:Receptor, Angiotensin, Type 1; D042461:Vascular Endothelial Growth Factor A