Objective: To investigate the effects of miR-106a-5p on the proliferation and migration of vascular endothelial cells, and the possible target gene of miR-106a-5p in endothelial cells. Methods: Human umbilical vein endothelial cells (HUVEC) were cultured in vitro, and the expression of mir-106a-5p in HUVECs was detected by real-time fluorescent quantitative polymerase chain reaction (RT-qPCR). Cell counting kit-8 (CCK-8) and wound healing assays were used to detected the proliferation and migration of HUVECs respectively.Dual luciferase repoter assay was used to identify the possible target gene of miR-106a-5p--STAT3. Results: mir-106a-5p inhibited the proliferation function of HUVECs (F=13.62, P<0.01). And mir-106a-5p expressed the migration of HUVEC,the closure rate in the mimic group was reduced after 12 h and 24 h of scratching (49.93/31.31) (χ(2)=8.240, P<0.05), (78.87/44.80) (χ(2)=10.50, P<0.01). The direct target gene of mir-106a-5p was STAT3, and miR-106a-5p regulated the expression of STAT3 through post-transcriptionally controlling. Conclusion: mir-106a-5p could inhibit proliferation and migration of HUVEC, and the possible target gene was STAT3.
目的: 探讨miR-106a-5p对血管内皮细胞的增殖、迁移功能的调控作用,及miR-106a-5p调节内皮细胞功能的可能作用靶点。 方法: 体外培养人脐静脉内皮细胞(HUVEC),通过逆转录实时荧光定量聚合酶链反应检测miR-106a-5p在HUVEC内的表达;并通过CCK-8实验、划痕实验检测miR-106a-5p对HUVEC增殖、迁移功能的影响;通过双荧光素酶实验及蛋白印记实验验证miR-106a-5p调节内皮细胞功能的可能靶点——信号转导与转录活化因子3(STAT3)。 结果: miR-106a-5p可抑制HUVEC的增殖功能(F=13.62,P<0.01)。同时miR-106a-5p可抑制HUVEC的迁移功能:划痕12 h后,模拟物组的划痕闭合率下调(49.93/31.31)(χ(2)=8.240,P<0.05);划痕24h后,模拟物组的划痕闭合率下调(78.87/44.80)(χ(2)=10.50,P<0.01)。miR-106a-5p的直接靶基因为STAT3,并通过转录后作用调控STAT3的表达。 结论: miR-106a-5p抑制HUVEC的增殖及迁移功能,其可能的作用靶基因为STAT3。.
Keywords: Atherosclerosis obliterans; Human umbilical vein endothelial cells; microRNA-106a-5p.