Abstract
Abstract: :
Purpose: To characterize an in vivo mouse model for the study of recurrent corneal erosion syndrome (RCES). Methods: Initially, a single in vivo manual, corneal epithelial debridement wound was created on the ocular surface of Balb/C mice; two wound sizes (1.5 and 2.5mm) were studied at various times after wounding. Corneas were either processed for whole mounts and stained with propidium iodide and an antibody against α9 integrin, or processed for analyses of cell proliferation using bromodeoxyuridine. In another experiment, the history of corneal healing was analyzed from 1 to 6 weeks after debridement wounding. Eyes were then processed for study by immunofluorescence, using both whole mounts and tissue sections for studies with antibodies against α3, α9, and ß4 integrins, as well as tenascin–C. Results: Whole mount microscopy results showed that recurrent erosions were common in young mice at time points past 1 week after both small and large wounding; 13 of 16 eyes studied developed signs of erosion, the frequency of which were the same for both small and large wounds. Corneas from mice with documented RCES showed both retention of α9 integrin and tenascin–C expression at the anterior stromal:epithelial interface as well as impaired relocalization of α3ß1 integrin to the basement membrane zone. Furthermore, after large wounding, RCES corneas frequently showed numerous goblet–like cells adjacent to a region of limbal basal cells that completely lacked α9 integrin. Conclusions: These data show that spontaneous recurrent corneal erosions occur in a mouse model after creation of a single manual debridement wound, and that α9 integrin localization is altered in mice suffering from RCES.
Keywords: cornea: epithelium • wound healing • cell adhesions/cell junctions