39 research outputs found
Ultraviolet radiation and cornea
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