Detection of epithelial apoptosis in lenses with cataract.
Ανίχνευση κυτταρικής απόπτωσης στα επιθηλιακά κύτταρα του περιφακίου καταρρακτικών φακών
Χαρακίδας, Αντώνης Χρ
Purpose: To probe the presence of apoptosis in the epithelium of human lenses with non-congenital cataract as well as to assess cell proliferation, a predicted consequence of apoptotic cell death, in this specific cell population.
Material and Methods: DNA fragmentation was assessed using terminal digoxigenin-labeled dUTP nick end labeling (TUNEL) in capsulotomy specimens obtained from patients who underwent either extracapsular cataract extraction for the removal of adult-onset cataract (n=51) or clear lens extraction for the correction of high myopia (n=25). Cell proliferation was assayed in 23 epithelia of cataractous lenses, and 20 epithelia of non-cataractous lenses with the proliferation marker MIB1, a monoclonal antibody against the nuclear antigen Ki-67 that is detected throughout the cell cycle but is absent in the resting (G0) cell.
Results: TUNEL staining was observed in 25 (92,6%) specimens of cortical cataracts and in all 4 capsulotomy specimens of lenses with posterior subcapsular opacities, whereas cells undergoing apoptosis were identified in 2 (8%) of the epithelia from non-cataractous lenses. Non-significant apoptosis of single cells was traced in 5 of 20 specimens of nuclear cataracts. Only two MIB1-positive samples were identified, one of which was a capsule obtained during intracapsular cataract extraction.
Conclusions: The epithelium of human lenses with cortical or posterior subcapsular cataract undergoes low rate apoptotic death. This limited epithelial apoptosis is unlikely to result in any significant cell density decrease since epithelial gaps are likely to be replaced by cell proliferation at the germinative zone of the anterior lens capsule. Nevertheless, the accumulation of small-scale epithelial losses during lifetime may induce alterations in lens fiber formation and homeostasis and result in loss of lens transparence.