Szentmáry Nóra, Nagy Zoltán Zsolt, Resch Miklós, Szende Béla, Süveges Ildikó
1st Department of Ophthalmology, Semmelweis University, Budapest.
Pathol Res Pract. 2005;201(5):399-404. doi: 10.1016/j.prp.2005.04.003.
This study aimed at investigating the proliferation and apoptosis of corneal cells following photorefractive keratectomy (PRK) treatment. PRK (-6.0 D correction) was performed with the Asclepion-Meditec MEL70 G-scan excimer laser on the right eye of each of 33 rabbits under combined local and general anaesthesia. Animals were sacrificed at 4 h, 1, 4, 7, 14, 28, 56, and 112 days postoperatively, and corneal samples from these eight groups were examined histologically. Stromal cell proliferation was evaluated by immunocytochemical analysis of Ki67. Apoptosis was detected using the terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick-end labeling (TUNEL) assay method. The untreated left eyes served as controls. Ki67 positivity was detected in the upper stroma on day 1, 4, 7, and 14, and keratocyte apoptosis on day 1, 4, 7, and 14 after PRK, but not at an earlier or later time. Neither Ki67 positivity nor apoptotic activity was observed in the controls (untreated corneas). PRK was found to trigger proliferation and apoptosis of corneal keratocytes. The frequency and spatial distribution of keratocyte proliferation and apoptosis are likely to be important determinants of the corneal wound healing process, but the detailed regulatory mechanisms have not yet been characterized.
