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Masahide Kokado, Yuka Okada, Mizuki Goto, Kazushi Ishikawa, Takeshi Miyamoto, Osamu Yamanaka, Sakuhei Fujiwara, Shizuya Saika; Increased Fragility, Impaired Differentiation, and Acceleration of Migration of Corneal Epithelium of Epiplakin-Null Mice. Invest. Ophthalmol. Vis. Sci. 2013;54(5):3780-3789. doi: 10.1167/iovs.12-11077.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the effects of gene ablation of epiplakin on the homeostasis of corneal epithelium in mice.
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.
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.
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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