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

In the unwounded cornea, tenascin-C localizes to a short stretch of the bas ement membrane zone at the corneoscleral junction or limbus. To determine w hether 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 in tegrins (alpha 3, alpha 9, and beta 4) in the tenascin-C knockout corneas i s evaluated by producing polyclonal cytoplasmic domain antipeptide sera and performing immunofluorescence microscopy. In addition, we evaluate the loc alization of several other proteins involved in wound healing, including fi bronectin, laminin beta 1, nidogen/ entactin, and VCAM-1, in both the tenas cin knockout and wild-type mice. There are no differences in healing rate, scarring, or neovascularization after corneal debridement wounds. (alpha 9 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 alpha 9 again becomes r estricted to the limbal border. Results show that tenascin-C is not require d for development or maintenance of the corneal limbus or for normal re-epi thelialization of corneal epithelial cells after debridement wounding.