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Oxidative stress contributes to the formation of cataracts. The leucine rich repeat containing G protein-coupled receptor 4 (LGR4, also known as GPR48), is important in many developmental processes. Since deletion of  Lgr4  has previously been shown to lead to cataract formation in mice, we sought to determine the specific role that  Lgr4  plays in the formation of cataracts. Initially, the lens opacities of  Lgr4 −/−   mice at different ages without ocular anterior segment dysgenesis (ASD) were evaluated with slit-lamp biomicroscopy. Lenses from both  Lgr4 −/−   and wild-type mice were subjected to oxidation induced protein denaturation to assess the ability of the lens to withstand oxidation. The expression of antioxidant enzymes was evaluated with real-time quantitative PCR. Phenotypically,  Lgr4 −/−   mice showed earlier onset of lens opacification and higher incidence of cataract formation compared with wild-type mice of similar age. In addition,  Lgr4 −/−   mice demonstrated increased sensitivity to environmental oxidative damage, as evidenced by altered protein expression. Real-time quantitative PCR showed that two prominent antioxidant defense enzymes, catalase (CAT) and superoxidase dismutase-1 (SOD1), were significantly decreased in the lens epithelial cells of  Lgr4 −/−   mice. Our results suggest that the deletion of  Lgr4  can lead to premature cataract formation, as well as progressive deterioration with aging. Oxidative stress and altered expression of several antioxidant defense enzymes contribute to the formation of cataracts.

Targeted Deletion of the Murine Lgr4 Gene Decreases Lens Epithelial Cell Resistance to Oxidative Stress and Induces Age-Related Cataract Formation