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  • Title: Increased fragility, impaired differentiation, and acceleration of migration of corneal epithelium of epiplakin-null mice.
    Author: Kokado M, Okada Y, Goto M, Ishikawa K, Miyamoto T, Yamanaka O, Fujiwara S, Saika S.
    Journal: Invest Ophthalmol Vis Sci; 2013 May 01; 54(5):3780-9. PubMed ID: 23599337.
    Abstract:
    PURPOSE: To investigate the effects of gene ablation of epiplakin on the homeostasis of corneal epithelium in mice. METHODS: Light and transmission electron microscopic histology, immunohistochemistry, and real-time RT-PCR were carried out to evaluate the effects of the loss of epiplakin on structure and gene expression of cell-cell adhesion-related components in mice. Integrity against mechanical intervention and wound-healing response of corneal epithelium were also tested. RESULTS: Epiplakin protein was detected in the cells of the basal layer of corneal epithelium. Morphologically basal-like cells were observed in the suprabasal layer of adult epiplakin-null corneal epithelium, suggesting an impaired intraepithelial cell differentiation. Such abnormality was not detected in mice before the age of postnatal day 14. Epiplakin-deficient epithelium exhibits fragility against mechanical intervention as compared with wild-type epithelium. Although cell proliferation is suppressed, migration-dependent wound healing is promoted in epiplakin-null epithelium. E-cadherin expression was suppressed by the loss of epiplakin in the epithelium. CONCLUSIONS: Lacking epiplakin affects cell differentiation of the corneal epithelium, as well as its proliferation activity and its structural integrity. The mechanism of acceleration of cell migration in the epiplakin-null corneal epithelium is to be further investigated, although suppression of expression of E-cadherin might be included.
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