MicroRNA-296 mediated corneal neovascularization in an animal model of corneal burns after alkali exposures.

Alkali burns of the cornea may lead to permanent visual impairment or complete blindness. In the current study, the role of microRNA 296 (miR-296) was explored in mouse corneal neovascularization induced by alkali burns. An alkali burn model in Balb/c mice was developed to study chemical corneal injuries. The expression of the miR-296 gene was measured by reverse-transcription-quantitative polymerase chain reaction. Fibroblast growth factor 23 (FGF23) protein expression was measured by western blot analysis. Possible impacted pathways were analyzed by Kyoto Encyclopedia of Genes and Genomes pathway analysis. miR-296 gene expression was examined following chemical corneal injury and it was demonstrated that different topical eye medications decreased miR-296 gene expression. miR-296 may participate in cytokine-cytokine receptor interaction pathways to influence corneal inflammatory responses. It was also revealed that FGF23 was expressed following chemical corneal injury and that different treatments with topical eye drops decreased its expression. miR-296 is a novel molecular modulator for alkali burns in the mouse cornea.