Reduced angiogenesis and delay in wound healing in angiotensin II type 1a receptor-deficient mice
Reduced angiogenesis and delay in wound healing in angiotensin II type 1a receptor-deficient mice
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DOI：
10.1016/j.biopha.2009.01.001
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发表时间：
2009-11-01
影响因子：
7.5
通讯作者：
Majima, Masataka
中科院分区：
文献类型：
--
作者：
Kurosaka, Maya;Suzuki, Tatsunori;Majima, Masataka
血管紧张素II（Angiotensin II，Ang II）是一种生物活性肽，在血压调节和盐-水平衡中起重要作用。近年来，研究发现血管紧张素Ⅱ具有促进血管生成的作用。由于伤口愈合过程高度依赖于血管生成，我们采用Ang II受体敲除小鼠（AT 1a（-/-））来研究Ang II是否通过AT 1a受体信号促进血管生成和伤口愈合。与野生型（WT）小鼠相比，AT 1a（-/-）小鼠的伤口愈合和伤口诱导的血管生成受到显著抑制，这些小鼠的伤口肉芽组织中CD 31表达降低。与溶剂处理的小鼠相比，用AT 1-R拮抗剂处理的小鼠的伤口愈合显著延迟，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，血管紧张素Ⅱ-AT 1a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。(C)2009年Elsevier Masson SAS。All rights reserved.
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.