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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Deletion of neuropeptide Y (NPY) 2 receptor in mice results in blockage of NPY-induced angiogenesis and delayed wound healing
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Deletion of neuropeptide Y (NPY) 2 receptor in mice results in blockage of NPY-induced angiogenesis and delayed wound healing

机译：小鼠中神经肽Y（NPY）2受体的缺失导致NPY诱导的血管生成受阻，伤口愈合延迟

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摘要

Neuropeptide Y (NPY), a 36-aa peptide, is widely distributed in the brain and peripheral tissues. Whereas physiological roles of NPY as a hormoneeurotransmitter have been well studied, little is known about its other peripheral functions. Here, we report that NPY acts as a potent angiogenic factor in vivo using the mouse corneal micro-pocket and the chick chorioallantoic membrane (CAM) assays. Unlike vascular endothefial growth factor (VEGF), mkrovessels induced by NPY had distinct vascular tree-like structures showing vasodilation. This angiogenic pattern was similar to that induced fay fibrobiast growth factor-2, and the angiogenic response was dose-dependent. In the developing chick embryo, NPY stimulated vascular sprouting from preexisting blood vessels. When [Leu~(31)Pro~(34)]NPY, a NPY-based analogue lacking high affinity for the NPY Y_2 receptor but capable of stimulating both Y_1 and Y_5 receptors, was used in the corneal model, no angiogenic response could be detected. In addition, NPY failed to induce angiogenesis in Y_2 receptor-null mice, suggesting that this NPY receptor subtype was mediating the angiogenic signal. In support of this finding, the Y_2 receptor, but not Y_1f Y_4, or Y_5 receptors, was found to be widely expressed in newly formed blood vessels. Further, a delay of skin wound healing with reduced neovascularization was found in Y_2 receptor-null mice. These data demonstrate that NPY may play an important role in the regulation of angiogenesis and angiogenesis-dependent tissue repair.
机译：神经肽Y（NPY）是一种36氨基酸的肽，广泛分布于大脑和周围组织。尽管已经很好地研究了NPY作为激素/神经递质的生理作用，但对其其他外周功能知之甚少。在这里，我们报告使用小鼠角膜微囊和鸡绒膜尿囊膜（CAM）测定法，NPY在体内起有效血管生成因子的作用。与血管内皮生长因子（VEGF）不同，NPY诱导的mkrovessels具有明显的血管树状结构，显示出血管舒张。该血管生成模式类似于诱导的费伊纤维增强生物生长因子-2，并且血管生成反应是剂量依赖性的。在发育中的雏鸡胚胎中，NPY刺激了原有血管的血管萌芽。当[Leu〜（31）Pro〜（34）] NPY（一种对NPY Y_2受体缺乏高亲和力但能够刺激Y_1和Y_5受体的基于NPY的类似物）用于角膜模型时，就不会产生血管生成反应检测到。此外，NPY未能诱导Y_2受体无效小鼠的血管生成，表明该NPY受体亚型介导了血管生成信号。为了支持该发现，发现Y_2受体而不是Y_1f Y_4或Y_5受体在新形成的血管中广泛表达。此外，在Y_2受体无效的小鼠中发现了具有减少的新血管形成的皮肤伤口愈合的延迟。这些数据表明，NPY可能在调节血管生成和依赖血管生成的组织修复中起重要作用。

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