Effects of angiotensin II skin wound healing receptor signaling during
Effects of angiotensin II skin wound healing receptor signaling during
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DOI：
10.1016/s0002-9440(10)63422-0
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发表时间：
2004-11-01
影响因子：
6
通讯作者：
Kondo, S
中科院分区：
文献类型：
--
作者：
Takeda, H;Katagata, Y;Kondo, S
组织血管紧张素（tissue angiotensin，Ang）系统独立于循环中的肾素-血管紧张素系统发挥作用，在心脏和肾脏的组织修复中发挥重要作用。在皮肤中，伤口加热系统的作用仍有待确定。我们的研究表明，口服选择性血管紧张素Ⅱ 1型受体（AT（1））阻滞剂抑制角质形成细胞再上皮化和血管生成在皮肤伤口愈合大鼠。免疫沉淀和Western印迹分析表明，在培养的角质形成细胞和肌成纤维细胞中存在AT（1）和AngII 2型受体（AT（2））。在溴脱氧尿苷掺入研究中，AT（1）信号的诱导增强了角质形成细胞和肌成纤维细胞的掺入。伤口愈合迁移试验显示，AT（1）信号的诱导加速角质形成细胞的再上皮化和肌成纤维细胞的恢复。在这些实验中，AT（2）信号的诱导作用反之亦然。综上所述，我们的研究表明，皮肤伤口愈合是由AT（1）和AT（2）之间的相反信号平衡调节的。
The tissue angiotensin (Ang) system, which acts independently of the circulating renin Ang system, is supposed to play an important role in tissue repair in the heart and kidney. In the skin, the role of the system for wound heating has remained to be ascertained. Our study demonstrated that oral administration of selective AngII type-1 receptor (AT(1)) blocker suppressed keratinocyte re-epithelization and angiogenesis during skin wound healing in rats. Immunoprecipitation and Western blot analysis indicated the existence of AT(1) and AngII type-2 receptor (AT(2)) in cultured keratinocytes and myofibroblasts. In a bromodeoxyuridine incorporation study, induction of AT(1) signaling enhanced the incorporation into keratinocytes and myofibroblasts. Wound healing migration assays revealed that induction of AT(1) signaling accelerated keratinocyte re-epithetization and myofibroblasts recovering. In these experiments, induction of AT(2) signaling acted vice versa. Taken together, our study suggests that skin wound healing is regulated by balance of opposing signals between AT(1) and AT(2).