Department of Pharmacology, Kitasato University School of Medicine, Kanagawa, Japan.
Biomed Pharmacother. 2009 Nov;63(9):627-34. doi: 10.1016/j.biopha.2009.01.001. Epub 2009 Feb 14.
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.
血管紧张素 II（Ang II）是一种生物活性肽，在血压调节和水盐平衡中发挥重要作用。最近有报道称，Ang II 可促进血管生成。由于伤口愈合过程高度依赖于血管生成，我们利用血管紧张素 II 受体敲除小鼠（AT1a(-/-)）来研究 Ang II 是否通过 AT1a 受体信号促进血管生成和伤口愈合。与野生型（WT）小鼠相比，AT1a(-/-)小鼠的伤口愈合和伤口诱导的血管生成明显受到抑制，并且这些小鼠的伤口肉芽组织中 CD31 的表达减少。与载体处理的小鼠相比，用 AT1-R 拮抗剂处理的小鼠的伤口愈合明显延迟，并且这种延迟伴随着伤口肉芽组织中血管内皮生长因子的表达减少。这些发现表明 Ang II-AT1a 信号在伤口愈合和伤口诱导的血管生成中起着至关重要的作用。
