Superoxide Dismutase-1 Regulates Corneal Neovasculalization in Mice

Abstract

Purpose: : Although corneal avascularity is indispensable for proper visual performance, its molecular mechanism remains unclear. It is reported that oxidative stress is involved in several diseases via redox-sensitive transcription factors including nuclear factor-kappa B (NF-kB) which play a central role of inflammation. Superoxide dismutase-1 (SOD-1) is a well known antioxidant enzyme, however, the role of SOD-1 in corneal avascularity is unknown. In this study, we determined the involvement of SOD-1 in corneal neovascularization (NV) utilizing SOD-1 deficient mice.

Methods: : Total corneal epithelium of SOD-1 deficient mice (KO) or wild type mice (WT) were removed after applying 0.15N NaOH to establish the animal model of alkali burn. NV areas were visualized by ConA lectin cardiac infusion.

Results: : Six days after alkali burn, NV area of KO (49.2±12.1%, n = 6) was significantly (P < 0.01) increased compared with WT (29.5±6.8%, n =8).

Conclusions: : This data indicated that SOD-1 regulates corneal neovascularization in alkali burn model, suggesting the possibility of antioxidant therapy for the maintenance of the transparency of the cornea.

Keywords: cornea: basic science • neovascularization • oxidation/oxidative or free radical damage