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. 2007 Oct 31;2(10):e1087. doi: 10.1371/journal.pone.0001087

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Zhang, Tseng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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The model asserts that cell proliferation and cell adhesion are major processes and E-cadherin a molecular regulator in maintaining corneal epithelium homeostasis. The model also proposes a regulatory feedback loop in controlling corneal epithelial thickness. Any perturbation (e.g., thinning) in corneal thickness would be counterbalanced by adjustment in the rate of cell proliferation. The model is based on previous reports on null mutations of Pax6, KFL4, AP2alpha, HMGN1 and this work (Bnc1) (See text for the description).