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Publication : Integrin expression during epithelial migration and restratification in the tenascin-C-deficient mouse cornea.

First Author  Sta Iglesia DD Year  2000
Journal  J Histochem Cytochem Volume  48
Issue  3 Pages  363-76
PubMed ID  10681390 Mgi Jnum  J:66121
Mgi Id  MGI:1928004 Doi  10.1177/002215540004800306
Citation  Iglesia DD, et al. (2000) Integrin expression during epithelial migration and restratification in the tenascin-C-deficient mouse cornea. J Histochem Cytochem 48(3):363-76
abstractText  In the unwounded cornea, tenascin-C localizes to a short stretch of the basement membrane zone at the corneoscleral junction or limbus. To determine whether the function of the limbus is affected by the absence of tenascin-C, mice possessing a deletion of tenascin-C and strain-matched wild-type mice are used in corneal debridement wounding experiments. The expression of integrins (alpha3, alpha9, and beta4) in the tenascin-C knockout corneas is evaluated by producing polyclonal cytoplasmic domain antipeptide sera and performing immunofluorescence microscopy. In addition, we evaluate the localization of several other proteins involved in wound healing, including fibronectin, laminin beta1, nidogen/entactin, and VCAM-1, in both the tenascin knockout and wild-type mice. There are no differences in healing rate, scarring, or neovascularization after corneal debridement wounds. alpha9 integrin is expressed at the limbal border of unwounded tenascin-C knockout animals and is upregulated during migration only after the larger wounds. At 8 weeks after larger wounds, the localization of alpha9 again becomes restricted to the limbal border. Results show that tenascin-C is not required for development or maintenance of the corneal limbus or for normal re-epithelialization of corneal epithelial cells after debridement wounding.
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