Rongrong Zong1, Tong Zhou2, Zhirong Lin3, Xiaorui Bao1, Yanghui Xiu4, Yanfeng Chen1, Longlong Chen3, Jian-xing Ma5, Zuguo Liu6, Yueping Zhou1. 1. Eye Institute of Xiamen University Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Xiamen, Fujian, China. 2. Department of Pharmacy, Zhangzhou Municipal Hospital of Fujian Province, Zhangzhou, Fujian, China. 3. Xiamen Eye Center Affiliated to Xiamen University, Xiamen, Fujian, China. 4. Xiamen Eye Center Affiliated to Xiamen University, Xiamen, Fujian, China 4Department of Ophthalmology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China. 5. Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States. 6. Eye Institute of Xiamen University Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Xiamen, Fujian, China 3Xiamen Eye Center Affiliated to Xiamen University, Xiamen, Fujian, China.
Abstract
PURPOSE: Although microRNA-184 (miR-184) is abundantly expressed in the corneas, the role of miR-184 in corneal neovascularization remains unknown. Here we investigated the association between miR-184 expression and corneal neovascularization. METHODS: Quantitative real-time PCR assay was conducted to detect the expression of miR-184 and its potential target genes in the corneal epithelium of rats with corneal suture-induced neovascularization. MicroRNA-184 was also applied topically to the suture rats. Mimic and inhibitor of miR-184 were transfected into the cultured human umbilical vein endothelial cells (HUVECs), human corneal epithelial (HCE) cells, and simian choroidal endothelial cells (RF/6A). The following experiments were performed to evaluate the effects of miR-184 in these transfected cells: cell proliferation by cell viability assay, cell migration by a scratch wound test, VEGF-induced tube formation, and VEGF and β-catenin levels by Western blot analysis. RESULTS: The expression of miR-184 was significantly reduced, whereas the gene expression of frizzled-4, a receptor of the Wnt pathway, was up-regulated in the corneal epithelium of corneal suture rats. The corneal neovascularization induced by suture was ameliorated by topical administration of miR-184. In the cells transfected with mimic and inhibitor of miR-184, miR-184 significantly suppressed the cell proliferation and cell migration of HUVECs, miR-184 down-regulated VEGF, and β-catenin expression in HUVECs and HCE cells. Furthermore, miR-184 inhibited the tube formation of RF/6A cells. CONCLUSIONS: Down-regulation of miR-184 is associated with up-regulation of VEGF and Wnt/β-catenin expression as well as corneal neovascularization, indicating that miR-184 negatively regulates corneal neovascularization.
PURPOSE: Although microRNA-184 (miR-184) is abundantly expressed in the corneas, the role of miR-184 in corneal neovascularization remains unknown. Here we investigated the association between miR-184 expression and corneal neovascularization. METHODS: Quantitative real-time PCR assay was conducted to detect the expression of miR-184 and its potential target genes in the corneal epithelium of rats with corneal suture-induced neovascularization. MicroRNA-184 was also applied topically to the suture rats. Mimic and inhibitor of miR-184 were transfected into the cultured human umbilical vein endothelial cells (HUVECs), humancorneal epithelial (HCE) cells, and simian choroidal endothelial cells (RF/6A). The following experiments were performed to evaluate the effects of miR-184 in these transfected cells: cell proliferation by cell viability assay, cell migration by a scratch wound test, VEGF-induced tube formation, and VEGF and β-catenin levels by Western blot analysis. RESULTS: The expression of miR-184 was significantly reduced, whereas the gene expression of frizzled-4, a receptor of the Wnt pathway, was up-regulated in the corneal epithelium of corneal suture rats. The corneal neovascularization induced by suture was ameliorated by topical administration of miR-184. In the cells transfected with mimic and inhibitor of miR-184, miR-184 significantly suppressed the cell proliferation and cell migration of HUVECs, miR-184 down-regulated VEGF, and β-catenin expression in HUVECs and HCE cells. Furthermore, miR-184 inhibited the tube formation of RF/6A cells. CONCLUSIONS: Down-regulation of miR-184 is associated with up-regulation of VEGF and Wnt/β-catenin expression as well as corneal neovascularization, indicating that miR-184 negatively regulates corneal neovascularization.
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