| Objective To investigate the expression and mechanism ofmiR-184on cornea neovascularization induced by alkali burning，and the influence on angiogenesis in vitro. Methods corneaneovascularization(CRNV) was induced by alkali burning. HUVECwas cultured in three-dimensional Matrigel. qRT-PCR wasperformed to analyze microRNA-184expression in vivo and invitro. Predicted and analyzed the target genes of microRNA-184by bioinformatics method. MicroRNA-184mimic was transfectedinto HUVEC together with liposome in vitro. Their effects on cellproliferation and migration was tested by MTT assay andTranswell migration assay, and tube formation was observed usingthe three-dimensional culture system on Matrigel. ResultsDelvelop a model for angiogenesis both in vivo and in vitro. Theexpression of miR-184on CRNV (0.145±0.013) was sigificantlyless than transparent cornea (1.015±0.189)(P＜0.01), and was just absolutely miniscule on HUVEC(0.007±0.004)(P＜0.05).The targets of miR-184predicted was associated with VEGFsingaling pathways. OD value of HUVEC （0.50±0.039）and thenumber of cells migrating through the transwell membranes（55.4±5.857）after transfection was reduced dramaticallycompared with the control groups （P＜0.01）, There was asignificant difference in the total branch point of capillarytube structures of HUVEC transfected into miR-184mimic（13.33±2.082）（P＜0.05）. Conclusion The marked decrease ofmiR-184expression during angiogenesis and target predictionsuggest a potential role and mechanism of miR-184played by VEGFsingaling pathways on CRNV. miR-184can supress the ability ofcell proliferation, migration and tube formation on Matrigel,and may participate in regulating the angiogenesis andmaintaining the corneal avascularity. |
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