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Abstract
Heterozygous deficiency in the Pax6 gene results in the analogous condition of aniridia in humans and small eye (Sey) in mice. The underlying pathogenesis is incompletely understood. An in vivo, murine, corneal wounding model was developed to study healing capacity, evaluate the limbal progenitor cell population (p63), and explore the role of soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) in aniridia related keratopathy. Results demonstrated a statistically significant delay in corneal wound healing in Sey mice at days 2 and 3 when compared to WT mice (p<0.05). There was no significant difference in corneal p63 staining (p>0.05). All corneas exhibited comparable sVEGFR-1 staining. In conclusion, our in vivo wounding model revealed delayed corneal healing in Sey mice that does not appear to be due to deficiency in p63 cellular expression. The comparable expression of sVEGFR-1 suggests that it alone is likely not responsible for corneal vascularization present in Sey mice.