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H. L. Chandler, K. M. Newkirk, A. E. Parent, C. M. H. Colitz, D. A. Wilkie, D. F. Kusewitt; Morphologic Characterization of UV-Induced Degeneration of the Cornea in Wild Type 129 Mice. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3504.
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© ARVO (1962-2015); The Authors (2016-present)
To characterize the histomorphology of chronic UV-induced corneal degeneration in wild type 129 mice.
All research reported was conducted in compliance with the ARVO statement for the use of animals in ophthalmic and vision research. Wild type 129 mice were exposed to 3200 J/m2 (2 minimal erythemal doses, MED) of UVR from a filtered Westinghouse FS-40 lamp three times a week for 50 wks. In a subsequent acute study, wild type 129 mice were exposed to 4800 J/m2 (3MED) and sacrificed at 12, 24, 48, 72, 96 hrs and 1 wk after UVR. Mice were examined clinically using slit microscopy. Following euthanasia, eyes were removed and fixed in 10% neutral buffered formalin.
All of the mice developed variable degrees of unilateral or bilateral corneal stromal thinning that often progressed to globe rupture. In some cases clefts/bullae were apparent in the corneal stroma by slit microscopy. Histologically, the early corneal lesions were characterized by loss of keratocytes, hyalinization and coagulation of the stromal collagen, without apparent inflammatory cell infiltration. In severe cases, stromal clefts and corneal rupture with subsequent inflammation and fibrosis were present. By histology, mice that received UVR exposure and their age matched controls demonstrated variable degrees of cataract formation. The majority of the cataracts in both groups were characterized by swelling of the posterior cortical lens fibers without evidence of proliferation, metaplasia or posterior migration of the lens epithelial cells. In an acute UV study all eyes appeared normal by slit microscopy before and after UVR exposure, with no evidence of corneal edema or ulceration. Histologically and by staining for cleaved caspase 3, apoptotic cells were present in the corneal epithelium at 12, 24 and 48 hrs post-UVR; rarely, apoptotic keratocytes were apparent. There were no lenticular changes seen in the acute UV study.
Similar degenerative lesions of the cornea have not been reported. The pathogenesis of these lesions is uncertain; however, the acute study demonstrates a possible role for UVR-induced apoptosis of corneal stromal cells in the progressive loss of keratocytes and subsequent coagulation and thinning of the corneal stroma. In this study, UVR did not induced cataractogenesis, as cataracts were observed in both UV-exposed and unexposed mice.
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