可溶性酪氨酸激酶2融合蛋白对肿瘤坏死因子α诱导腹膜血管内皮细胞新生血管能力的影响

目的观察可溶性酪氨酸激酶2融合蛋白（sTie-2-Fc）对肿瘤坏死因子α（TNF-α）诱导腹膜血管内皮细胞新生血管能力的影响，及探讨TNF-α促进血管新生的机制。方法观察原代培养的人腹膜微血管内皮细胞经TNF-α作用后在基底膜基质（Matrigel）上形成管状结构的能力；在transwell板上迁移能力；对异硫氰酸荧光素标记的牛血清白蛋白（FITC-BSA）通透性的改变；以及用sTie-2-Fc干预后细胞上述功能的改变。结果TNF-α组与对照组相比，内皮细胞形成管状结构数显著增多（70±7）个，4个视野比（17±4）个，4个视野，P〈0．05]；TNF-α＋sTie-2-Fc组（40±6）个，4个视野]比TNF-α组管状结构数显著减少（P〈0．05）；sTie-2／Fc组和对照组间细胞管状结构数差异无统计学意义。TNF-α促进内皮细胞迁移能力可被sTie-2-Fc拮抗（198±12）个／HP比（76±11）个／HP，P〈0．05]。对照组和sTie-2-Fc组间通透性差异无统计学意义；与对照组和sTie-2-Fc组比较，TNF-α组和TNF-α＋sTie-2-Fc组细胞通透性显著增加（P〈0．05），但两组间细胞通透性差异也无统计学意义。结论TNF-α促进腹膜血管新生与血管生成素及其受体有关。

Effect of sTie-2-Fc on TNF-α-induced angiogenesis of human omental tissue microvascular endothelial cells

Objective To observe the effect of sTie-2-Fc on TNF-α-induced angiogenesis of human omental tissue microvascular endothelial cells（HOTMEC）and explore the mechanism of angiogenesis induced by TNF-α. Methods HOTMEC was suspended in complete medium as control group and complete medium with TNF-α or TNF-α plus sTie-2-Fc or sTie-2-Fc only as experiment groups respectively. Then the capability of tube formation in Matrigel and migration in transwell plate as well as the permeability change to FITC labeled BSA of HOTMEC were observed. Results HOTMEC showed a typical cobblestone growth pattern and immunocytochemistry staining for Ⅷ factor was positive. As compared to the control, TNF-α promoted tube formation （70±7） vs（17±4）tube/4 fields, P<0.05] and migration（198±12） vs(38±7) cell/HP] of HOTMEC, meanwhile, such effects could be inhibited by sTie-2-Fc （40±6）tube/4 fields, (76±11) cell/HP, P<0.05]. TNF-α could also enhance the permeability of HOTMEC, which could not be inhibited by sTie-2-Fc. Conclusion Angiopoietin-Tie-2 may contribute to angiogenesis in peritoneum by promoting tube formation and migration of HOTMEC in long-term PD patients