Ultraviolet radiation and cornea

Abstract: Results. UVR at subthreshold doses did not produce any corneal damage that could be detected in the light microscope. Apoptosis was detected to be one important mechanism leading to corneal cell damage after UVR exposure at photokeratitis doses. Photokeratitis doses at 270, 280, and 290 inn led to a superficial corneal damage. Apoptotic cells were found only in the epithelial layer and superficial keratocytes. UVR exposure at photokeratitis doses at 310 inn resulted in severe corneal damage, where apoptosis was seen in the epithelium, the keratocytes through the whole corneal stromal thickness, and the endothelium. During the first seventy- six hours after exposure to 310 nm UVR at photokeratitis doses, keratocytes underwent apoptosis and disappeared. Keratocytes bordering this damaged cell-free area started to produce hyaluronan during the repopulation phase. The production of hyaluronan peaked at 7 days after UVR exposure. Fourteen days after exposure the corneas were completely restored, and only trace amounts of hyaluronan was detected close to the Descemet's membrane. Repeated exposures of the corneas to photokeratitis doses at 310 nm at 1 week intervals resulted in hyaluronan deposits in the corneal stroma, and reduction of the keratocyte apoptosis level. Fas ligand protein in the normal rabbit corneas was expressed only in epithelial and endothelial cells. UVR exposure of the corneas at photokeratitis doses resulted in Fas ligand protein expression also in keratocytes, suggesting the Fas/Fas ligand system activation leading to apoptosis. Biglycan gene was not expressed in the normal rabbit corneas. However, UVR exposure at photokeratitis doses activated a distinct biglycan gene expression at 7 days after exposure. Biglycan gene expression decreased 28 days after exposure. Conclusion. A photokeratitis dose of 310 rim UVR is needed to cause a significant keratocyte damage. A photokeratitis dose of the shorter wavelengths causes damage to epithelial cells and superficial keratocytes only, due to a very high absorption of these wavelengths in the epithelium. The keratocyte production of HA appears to be a sign of cell readiness to repopulate the damaged stroma devoid of keratocytes. Apoptosis, initiated by Fas/Fas ligand system activation, is a mechanism leading to the corneal cell death after UVR exposure. Repeated UVR exposures lead to increased production and accumulation of HA in the corneal stroma. The repopulated keratocytes are much more resistant to apoptosis than the native ones. HA accumulation may be a sign of long term changes in the cornea, leading to corneal degeneration. There is no expression of biglycan gene in the normal rabbit cornea. The UVR exposure leads to a strong expression of biglycan gene in the rabbit cornea that decreases 4 weeks after exposure indicating the biglycan involvement in the corneal repair process. Biglycan appears to be a novel marker of the corneal wound healing.