Impaired angiogenesis in neuropeptide Y (NPY)-Y2 receptor knockout mice
Impaired angiogenesis in neuropeptide Y (NPY)-Y2 receptor knockout mice
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DOI：
10.1016/s0196-9781(02)00281-4
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发表时间：
2003-01-01
期刊：
影响因子：
3
通讯作者：
Zukowska, Z
中科院分区：
文献类型：
--
作者：
Lee, EW;Grant, DS;Zukowska, Z
Y1-Y 5受体（Rs）介导的NPY的血管生成活性进行了研究，使用Y2 R-null小鼠和R-特异性拮抗剂。在Y2 R基因敲除小鼠中，NPY诱导的主动脉发芽和体内基质胶毛细血管形成减少了50%; Y1 R拮抗剂阻断了剩余的反应。在野生型小鼠中，Y2 R-（和Y 5 R-）拮抗剂同样抑制NPY诱导的发芽，但Y1 R-拮抗剂抑制较少。自发和NPY诱导的缺血腓肠肌血运重建在Y2 R基因敲除小鼠中同样减少。因此，NPY诱导的自发性和缺血性血管生成主要由Y2 Rs介导。然而，Y 5 Rs和Y1 Rs在较小程度上也可能在NPY介导的血管生成中起作用。(C)2002年爱思唯尔科技有限公司All rights reserved.
Which of Y1-Y5 receptors (Rs) mediate NPY's angiogenic activity was studied using Y2R-null mice and R-specific antagonists. In Y2R-null mice, NPY-induced aortic sprouting and in vivo Matrigel capillary formation were decreased by 50%; Y1R-antagonist blocked the remaining response. NPY-induced sprouting was equally inhibited by Y2R- (and Y5R-but less by Y1R-) antagonists in wild type mice. Spontaneous and NPY-induced revascularization of ischemic gastrocnemius muscles were similarly reduced in Y2R-null mice. Thus, NPY-induced angiogenesis, spontaneous and ischemic, is primarily mediated by Y2Rs. However, Y5Rs and, to a lesser degree Y1Rs, also may play a role in NPY-mediated angiogenesis. (C) 2002 Elsevier Science Inc. All rights reserved.