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Romana Kucerova, Jingxing Ou, Diane Lawson, Lucy J. Leiper, J. Martin Collinson; Cell Surface Glycoconjugate Abnormalities and Corneal Epithelial Wound Healing in the Pax6+/− Mouse Model of Aniridia-Related Keratopathy. Invest. Ophthalmol. Vis. Sci. 2006;47(12):5276-5282. doi: 10.1167/iovs.06-0581.
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purpose. Congenital aniridia due to heterozygosity for Pax6 is associated with ocular surface disease, including keratopathy. This study investigated how defects in glycoconjugate component of the cell surface of Pax6 +/− could cause the abnormal cellular migration phenotypes associated with the disease.
methods. Immunohistochemistry, lectin-based histochemistry, conventional staining techniques, and proteomic assays were performed on eyes and cultured corneal epithelial cells from wild-type and Pax6 +/ − littermates. Wild-type cells were manipulated in culture to replicate the glycoconjugate abnormalities found in Pax6 heterozygotes and determine the consequences for wound healing.
results. Multiple glycoconjugate defects were found in Pax6-mutant cells. Lectin cytochemistry of corneal epithelial cells suggested a partial failure of glycoprotein trafficking. Blocking cell surface carbohydrate moieties in wild-type corneal cells caused wound-healing delays similar to those seen in untreated Pax6 +/ − cells.
conclusions. Alterations to the cell surface glycoconjugate signature of Pax6 +/ − corneal epithelia restrict the ability of cells to initiate migration in response to wounding. This underlies the observed wound-healing delay in cultured Pax6 +/ − epithelia.
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