Localization of beta-catenin in Type II Diabetic murine corneal epithelial tissue before and after injury
Kalker, Molly K.
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The Center for Disease Control estimates that 9% of Americans have Type II Diabetes (CDC, 2020), which is a major risk factor for blindness. The delayed wound healing displayed in Type II Diabetes can cause corneal ulcers and persistent epithelial defects, among other conditions. While corneal transplants can be effective, they are not always available or appropriate. The protein Β-catenin plays an important role in the adherens junction, acting as a bridge between E-cadherin and a-catenin to indirectly anchor actin to E-cadherin. In healthy, unwounded epithelium, adherens junctions are generally localized to apical regions of tissue, and are maintained to attach cells together, which helps maintain epithelial integrity and cell shape. After wounding, adherens junctions are rearranged, with some Β-catenin being trafficked into the cytoplasm for degradation. This promotes cell migration and wound closure. This thesis investigates the localization of Β-catenin in the Type II Diabetic murine cornea before and after wounding. Our results indicated that epithelium from unwounded Type II Diabetic corneas showed apical localization of Β-catenin, but there was a lesser amount compared to control. After wounding, tissue was found to have an increase of Β-catenin at the wound edge in basal regions of the epithelium, but the extent of that increase varied by time after injury. With the exception of the 2-hour wound, however, a smaller amount of Β-catenin was found at the wound edge of Type II Diabetic mice, compared to control. In summary, there were many differences between the corneas of Type II diabetic and control corneas.