Blockade of vascular endothelial growth factor suppresses experimental restenosis after intraluminal injury by inhibiting recruitment of monocyte lineage cells
Blockade of vascular endothelial growth factor suppresses experimental restenosis after intraluminal injury by inhibiting recruitment of monocyte lineage cells
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DOI：
10.1161/01.cir.0000145123.85083.66
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发表时间：
2004-10-19
期刊：
影响因子：
37.8
通讯作者：
Sunagawa, K
中科院分区：
文献类型：
--
作者：
Ohtani, K;Egashira, K;Sunagawa, K
背景-通过递送血管内皮生长因子（VEGF）的治疗性血管生成已经引起了人们的关注。然而，血管内皮生长因子在实验性再狭窄（新生内膜形成）后血管腔内injure.Methods和Results-We报道，血管内皮生长因子的可溶性血管内皮生长因子受体1（sFlt-1）基因转移的阻断衰减后，在兔，大鼠和小鼠腔内损伤的新生内膜形成。sFlt-1基因转染可明显减轻早期血管炎症和增殖，以及后期的新生内膜形成。sFlt-1基因转移还抑制了炎症因子如单核细胞趋化蛋白-1和VEGF的表达增加。血管内VEGF基因转移增强血管外膜的血管生成，但没有减少neointimal formation. Conclusions增加VEGF的表达和活性是必不可少的实验性再狭窄的发展后，管腔内损伤招募单核细胞系细胞。
Background-Therapeutic angiogenesis by delivery of vascular endothelial growth factor (VEGF) has attracted attention. However, the role and function of VEGF in experimental restenosis (neointimal formation) after vascular intraluminal injury have not been addressed.Methods and Results-We report herein that blockade of VEGF by soluble VEGF receptor 1 (sFlt-1) gene transfer attenuated neointimal formation after intraluminal injury in rabbits, rats, and mice. sFlt-1 gene transfer markedly attenuated the early vascular inflammation and proliferation and later neointimal formation. sFlt-1 gene transfer also inhibited increased expression of inflammatory factors such as monocyte chemoattractant protein-1 and VEGF. Intravascular VEGF gene transfer enhanced angiogenesis in the adventitia but did not reduce neointimal formation.Conclusions-Increased expression and activity of VEGF are essential in the development of experimental restenosis after intraluminal injury by recruiting monocyte-lineage cells.