Vascular endothelial growth factor regulates reendothelialization and neointima formation in a mouse model of arterial injury
Vascular endothelial growth factor regulates reendothelialization and neointima formation in a mouse model of arterial injury
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DOI：
10.1161/01.cir.0000145120.37891.8a
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发表时间：
2004-10-19
期刊：
影响因子：
37.8
通讯作者：
Sauter, BV
中科院分区：
文献类型：
--
作者：
Hutter, R;Carrick, FE;Sauter, BV
背景--动脉损伤后，内皮再形成的速度对新生内膜的形成至关重要。血管内皮生长因子（VEGF）是一种有效的内皮细胞有丝分裂原，被认为可以加速经皮冠状动脉介入治疗后的内皮修复和防止内膜增生。然而，血管内皮生长因子治疗的确切作用机制和动脉损伤后内源性血管内皮生长因子的生理作用还没有很好的描述。为了更好地理解VEGF在动脉修复中的作用，我们过表达VEGF和一种可溶性嵌合VEGF受体。方法和结果-四组C57 BL/6小鼠在全身注射表达（1）VEGF，（2）VEGF-陷阱，（3）VEGF加VEGF-陷阱，或（4）对照腺病毒。基因转移后，腺病毒编码蛋白的循环水平显著升高。血管内皮生长因子过度表达促进动脉损伤后2周再内皮化和管腔内皮细胞增殖（P
Background-The rate of reendothelialization is critical in neointima formation after arterial injury. Vascular endothelial growth factor (VEGF), a potent endothelial mitogen, has been advocated for accelerating endothelial repair and preventing intimal hyperplasia after percutaneous coronary interventions. However, the precise mechanism of action of VEGF treatment and the physiologic role of endogenous VEGF after arterial injury are not well described. To better understand the role of VEGF in arterial repair, we overexpressed both VEGF and a soluble, chimeric VEGF receptor (VEGF-trap), which binds free VEGF with high affinity, in a mouse model of arterial injury.Methods and Results-Four groups of C57BL/6 mice underwent denuding endothelial injury 1 day after systemic injection of recombinant adenovirus expressing (1) VEGF, (2) VEGF-trap, (3) VEGF plus VEGF-trap, or (4) control adenovirus. Circulating levels of adenovirus-encoded proteins were significantly elevated after gene transfer. VEGF overexpression accelerated reendothelialization and increased luminal endothelial cell proliferation 2 weeks after arterial injury (P