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April 1989

Fibronectin and Corneal Epithelial Wound Healing in the Vitamin A-Deficient Rat

Author Affiliations

From the Eye Research Institute of Retina Foundation (Drs Frangieh, Hayashi, Teekhasaenee, Gipson, and Kenyon), the Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School (Drs Frangieh, Hayashi, Teekhasaenee, and Kenyon), and the Immunopathology Unit, Department of Pathology, Massachusetts General Hospital (Dr Colvin), Boston; and the Department of Applied Biological Sciences, Massachusetts Institute of Technology, Cambridge (Drs Frangieh, Hayashi, Teekhasaenee, Wolf, and Kenyon).

Arch Ophthalmol. 1989;107(4):567-571. doi:10.1001/archopht.1989.01070010581034

• The time course of the appearance of fibronectin (Fn) on wounded corneal surfaces was studied in vitamin A-deficient (A-) and pair-fed control rats. At various times following a central epithelial abrasion, the tissue was harvested, and Fn was localized on frozen corneal sections by an indirect immunofluorescence technique. There was no detectable Fn in intact, nonwounded control or intact A- corneas, except for Descemet's membrane. Within a half hour after abrasion, a band of Fn appeared on the denuded corneal surface of pair-fed control rats and became a continuous, prominent layer at four hours. This layer remained until 16 hours but disappeared at 24 hours when the epithelium had resurfaced over the defect. In severely A- rats, reepithelialization following central epithelial abrasion was delayed, and no Fn band was discernible at any time from one to 32 hours after injury. Light microscopy revealed a progressive increase in polymorphonuclear neutrophil infiltration with time in the underlying stroma in severely A- rats. This study indicated that in severe vitamin A deficiency, delayed epithelial migration is associated with an inflammatory cell layer and occurred in the absence of Fn.

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