新生血管形成过程中miR-296-5p对FGF23的调控作用

The Regulatory Effect of miR-296-5p on FGF23 During Neovascularization

目的研究miR-296-5p通过调节成纤维细胞生长因子23(FGF23)在新生血管生成过程中发挥的调控作用。方法用血管内皮生长因子(VEGF)诱导人脐静脉内皮细胞(HUVECs),构建模拟新生血管形成的体外模型,通过RT-qPCR比较对照组与新生血管组中miR-296-5p的表达水平。通过细胞转染构建miR-296-5p高表达组、miR-296-5p低表达组以及对照组细胞,比较3组细胞的迁移和成管能力,并通过蛋白免疫印迹实验比较3组FGF23的表达水平。结果与未经处理的对照组相比,VEGF诱导的新生血管组中miR-296-5p的表达水平显著增加(P<0.001)。与对照组比较,miR-296-5p低表达组的迁移距离和成管数均降低(P<0.001和P<0.05);而miR-296-5p高表达组的迁移距离和成管数均增加(P<0.001和P<0.01)。与对照组比较,miR-296-5p低表达组的FGF23表达水平明显降低(P<0.01);而miR-296-5p高表达组FGF23表达水平明显升高(P<0.01)。结论miR-296-5p可通过上调FGF23的表达促进新生血管生成。

Objective To investigate the regulatory role of miR-296-5p during neovascularization by modulating fibroblast growth factor 23(FGF23).Methods Human umbilical vein endothelial cells(HUVECs)were induced with vascular endothelial growth factor(VEGF)to construct an in vitro model simulating neovascularization.The expression levels of miR-296-5p in the control group and the neovascularization group were compared using RT-qPCR.3 groups of cells,namely the miR-296-5p overexpressed group,the miR-296-5p underexpressed group,and the control group,were constructed through cell transfection.The migration and vascularization of these 3 groups were compared,and the expression levels of FGF23 in the 3 groups were compared using Western blot.Results Compared with the untreated control group,the expression level of miR-296-5p was significantly increased in the VEGF-induced neovascularization group(P<0.001).Compared with the control group,the migration distance and the number of tubes formed were significantly reduced in the miR-296-5p underexpressed group(P<0.001 and P<0.05),while they were significantly increased in the miR-296-5p overexpressed group(P<0.001 and P<0.01).Compared with the control group,the expression level of FGF23 was significantly decreased in the miR-296-5p underexpressed group(P<0.01),while it was significantly increased in the miR-296-5p overexpressed group(P<0.01).Conclusion Our findings suggest that miR-296-5p can promote neovascularization by upregulating the expression of FGF23.