Effects of Vitamin D Receptor Knockout, Vitamin D Deficiency, and Diabetes on Corneal Epithelial Nerve Density
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This project is designed to test the hypothesis that vitamin D deficiency exacerbates preexisting primary corneal pathologies. Our lab has established that the corneal epithelium in diabetic mice heals at a faster rate than the epithelium in diabetic vitamin D receptor (VDR) knockout (KO) mice. It is known that within diabetic mice, the corneal nerve density is decreased, and it has been hypothesized that the decreased nerve density can slow corneal epithelium healing within mice. However, it is unknown how VDR KO or vitamin D deficiency in diabetic mice will affect corneal nerve density. In order to determine if nerve density is affected by VDR KO or vitamin D deficiency, mouse corneas were collected, nerves were immuno-stained for confocal microscope photography, and images were analyzed by image processing to determine nerve density. The results demonstrate that in otherwise healthy vitamin D deficient and VDR KO mice lacking the diabetic condition, nerve density was not affected by either vitamin D condition. Corneal nerve density was significantly decreased when vitamin D deficiency or VDR KO was combined with diabetes, confirming the hypothesis that vitamin D deficiency does worsen preexisting corneal pathologies. In addition, this finding may provide an explanation as to why diabetic VDR KO mice have delayed epithelial wound healing compared to control diabetic mice.