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

刘华长; 杨彦立; 薛增明; 任珊

doi:10.13898/j.cnki.issn.1000-2200.2021.12.006

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

摘要

摘要:
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。

Abstract:
ObjectiveTo 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.
MethodsThe HUVECs were divided into the NC group, IL-1β group, 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.
ResultsCompared 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-1β group(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).
ConclusionsInhibiting 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.

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