HKD5对人脐静脉内皮细胞游走及血管形成的抑制作用

目的:体外实验研究活化型高分子量激肽原（HKa）轻链富含组氨酸区域5 (HKD5)对人脐静脉内皮细胞（HUVECs）的粘附、游走及血管形成的影响。 方法:体外重组融合蛋白-活化型高分子量激肽原轻链富含组氨酸区域5 (GST-D5H)。WST-1法观察HUVECs细胞粘附能力；用改良Boyden Chamber膜侵袭系统观察HUVECs细胞游走(趋化)；用血管形成实验观察HUVECs细胞形成新生血管能力。 结果:GST-D5H作用后，HUVECs细胞粘贴率降低（P<0.05），游走穿膜细胞数明显低于对照组（P<0.01），诱导内皮细胞形成管腔数及长度均低于对照组（P<0.05）。 结论:GST-D5H能有效抑制HUVECs细胞粘附、游走，使该细胞粘附力降低，迁移性下降及血管形成数目减少或变细。

Domain 5 of active high molecular weight kininogen inhibits HUVEC adhesion, migration and angiogenesis

AIM: To study the effect of domain 5 of the active high molecular weight kininogen(HKa) on the vitronectin-mediated adhesion and migration and angiogenesis of human umbilical vein endothelial cells(HUVECs) in vitro.METHODS: Recombinant HK domain 5(GST-D5H) was prepared.WST-1 was used to study the effects of adhesiveness by GST-D5H on HUVECs.The Boyden Chamber membrane invasion culture system was used to study the migration,and tube formation was used to study angiogenesis.RESULTS: The adhesion rate was down regulated in GST-D5H group(P<0.05).In the membrane invasion culture system,the number of migrating HUVECs was significantly lower in GST-D5H group than that in control group(P<0.01).The number and length of tubes were significantly lower in GST-D5H group(P<0.05) than that in control.CONCLUSION: GST-D5H inhibits vitronectin-mediated adhesion,migration and angiogenesis of HUVECs in vitro.