Purpose To evaluate the roles of ADP-ribosylation factor (ARF) in alkali-induced corneal neovascularization (CNV).
Methods CNV was induced by alkali injury and compared in ARF inhibitor- or vehicle-treated mice three weeks after injury. Angiogenic and apoptosis factor expression in corneas after injury was quantified by RT-PCR. Human retinal endothelial cells (HRECs) apoptosis induced by ARF inhibitor were detected by flow cytometry.
Results The mRNA expression of ARF was augmented in the corneas after alkali injury. Compared with vehicle-treated mice, ARF inhibitor treated mice exhibited impaired CNV three weeks after injury, as evidenced by corneal whole mount CD31-staining. Concomitantly, the enhancement of intraocular VEGF expression was reduced in ARF inhibitor treated mice than in control mice after injury. Moreover, local administration of ARF inhibitor after alkali injury enhanced intraocular Caspase-3 expression. ARF inhibitor treatment can significantly induce HRECs apoptosis.
Conclusion ARF inhibitor can induce the regression of alkali-induced CNV through increased endothelial cell apoptosis and down regulated intracorneal VEGF expression. ARF is an effective intervention target for corneal neovascularization. |
