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Journal of Histochemistry and Cytochemistry, Vol. 48, 363-376, March 2000, Copyright © 2000, The Histochemical Society, Inc.
Integrin Expression During Epithelial Migration and Restratification in the Tenascin-C-deficient Mouse Cornea
Drina D. Sta Iglesiaa,
Purvi H. Galaa,
Tianqing Qiua, and
Mary Ann Steppa
a Department of Anatomy and Cell Biology and Department of Ophthalmology, The George Washington University Medical Center, Washington, DC
Correspondence to:
Mary Ann Stepp, Dept. of Anatomy and Cell Biology, The George Washington University Medical Center, 2300 I Street NW, Washington, DC 20037.
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 ( 3, 9, and ß4) 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 ß1, 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. 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 9 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.
(J Histochem Cytochem 48:363375, 2000)
Key Words:
tenascin-C, wound healing, integrins, re-epithelialization, cornea

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