miR-503-5p对IL-1β诱导的血管内皮细胞增殖、迁移、凋亡和黏附的影响

Effects of miR-503-5p on the proliferation,migration,apoptosis and adhesion of vascular endothelial cells induced by IL-1β

目的:探讨miR-503-5p对白细胞介素1β(IL-1β)诱导的血管内皮细胞增殖、迁移、凋亡和黏附的影响和分子机制。方法:将人脐静脉血管内皮细胞(HUVECs)分为NC组、IL-1β组、IL-1β+anti-miR-con组及IL-1β+anti-miR-503-5p组。分别采用噻唑蓝(MTT)法、黏附实验、流式细胞术、Transwell实验检测HUVECs增殖、黏附、凋亡和迁移能力。Western blotting检测细胞间黏附分子1(ICAM-1)、血管细胞黏附分子1(VCAM-1)表达水平。结果:与NC组比较,IL-1β组HUVECs细胞活力、迁移细胞数显著降低,细胞黏附数、凋亡率、ICAM-1和VCAM-1蛋白表达显著升高(P<0.01)。与IL-1β+anti-miR-con组比较,IL-1β+anti-miR-503-5p组HUVECs细胞活力、迁移细胞数显著升高,细胞黏附数、凋亡率、ICAM-1和VCAM-1蛋白表达显著降低(P<0.01)。结论:抑制miR-503-5p表达可促进血管内皮细胞增殖和迁移,抑制细胞黏附和凋亡,其机制可能与抑制ICAM-1和VCAM-1表达有关。

Objective:To explore the effects of miR-503-5p on the proliferation,migration,apoptosis and adhesion of human umbilical vein endothelial cells(HUVECs)induced by interleukin1β(IL-1β),and its molecular mechanism.Methods:The HUVECs were divided into the NC group,IL-1βgroup,IL-1β+anti-miR-con group and IL-1β+anti-miR-503-5p group.The proliferation,adhesion,apoptosis and migration ability of cells were detected using MTT assay,adhesion assay,flow cytometry and Transwell assay,respectively.The expression levels of intercellular adhesion molecule 1(ICAM-1)and vascular cell adhesion molecule 1(VCAM-1)were detected using Western blotting.Results:Compared with the NC group,the cell viability and migrated cell numbers of HUVECs significantly reduced,and the cell adhesion numbers,apoptosis rate,and ICAM-1 and VCAM-1 protein expression levels significantly increased in the IL-1βgroup(P<0.01).Compared with the IL-1β+anti-miR-con group,the cell viability and migrated cell numbers of HUVECs significantly increased,and the cell adhesion numbers,apoptosis rate,and ICAM-1 and VCAM-1 protein expression levels significantly decreased in the IL-1β+anti-miR-503-5p group(P<0.01).Conclusions:Inhibiting the miR-503-5p expression can promote the vascular endothelial cell proliferation and migration,and inhibit vascular adhesion and apoptosis,which may be related to the inhibition of ICAM-1 and VCAM-1 expression.