Browsing by Subject "Macular dystrophy"

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    Cell proliferation and apoptosis in stromal corneal dystrophies
    (Murcia : F. Hernández, 2007) Szentmáry, N.; Takács, L.; Berta, Andras; Szende, B.; Süveges, I.; Módis, L.
    The aim of our study was to evaluate corneal cell proliferation and apoptosis in cases of granular, macular and lattice dystrophy, and to provide evidence which may help to clarify whether apoptosis is a pathogenic factor in any of these dystrophies. The study group comprised 39 eyes (from 33 patients) which had undergone penetrating keratoplasty (PK) for stromal dystrophies: these comprised 12 eyes (from 9 patients, 55.5% males) with granular dystrophy, 13 eyes (12 patients, 33.3% males) with macular dystrophy, and 14 eyes (13 patients, 61.5% males) with lattice type I dystrophy. A further 4 corneal buttons from enucleated eyes of 4 patients with choroideal melanoma served as controls. Immunocytochemical analysis of Ki67 (DNAcon Kit, DakoCytomation A/S, Glostrup, Denmark) was used for evaluation of cell proliferation. Apoptosis was detected by use of the TUNEL (terminal deoxyribonucleotidyl transferase-mediated dUTPdigoxigenin nick-end labelling) assay method (Apoptag reagent, Q-Biogene, Strasbourg, France). Statistical comparisons were made using the Mann-Whitney test. No Ki67-positive cells were detected in the studygroup or control corneas. In control corneas no apoptotic activity was found. In the study group the mean (normalised) apoptotic keratocyte number was 1.1±1.7 in granular dystrophy and 0.5±1.1 in lattice type I The aim of our study was to evaluate corneal cell proliferation and apoptosis in cases of granular, macular and lattice dystrophy, and to provide evidence which may help to clarify whether apoptosis is a pathogenic factor in any of these dystrophies. The study group comprised 39 eyes (from 33 patients) which had undergone penetrating keratoplasty (PK) for stromal dystrophies: these comprised 12 eyes (from 9 patients, 55.5% males) with granular dystrophy, 13 eyes (12 patients, 33.3% males) with macular dystrophy, and 14 eyes (13 patients, 61.5% males) with lattice type I dystrophy. A further 4 corneal buttons from enucleated eyes of 4 patients with choroideal melanoma served as controls. Immunocytochemical analysis of Ki67 (DNAcon Kit, DakoCytomation A/S, Glostrup, Denmark) was used for evaluation of cell proliferation. Apoptosis was detected by use of the TUNEL (terminal deoxyribonucleotidyl transferase-mediated dUTPdigoxigenin nick-end labelling) assay method (Apoptag reagent, Q-Biogene, Strasbourg, France). Statistical comparisons were made using the Mann-Whitney test. No Ki67-positive cells were detected in the studygroup or control corneas. In control corneas no apoptotic activity was found. In the study group the mean (normalised) apoptotic keratocyte number was 1.1±1.7 in granular dystrophy and 0.5±1.1 in lattice type I controls, the difference was statistically significant only for macular dystrophy (1.6±1.2; p = 0.01). Keratocyte apoptosis seems to be a concomitant or pathogenic factor in macular dystrophy. However, the pathways that are triggered to result in increased apoptotic cell death remain to be clarified.
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    P21, p27, bax, cathepsin and survivin pathways in macular dystrophy corneas
    (Murcia : F. Hernández, 2010) Szentmáry, Nora; Stündl, Adrienn; Szende, Béla; Süveges, Ildiko
    The purpose of our study was to elucidatepathways of genetically programmed cell death(apoptosis) in corneas with macular dystrophy.10 corneal buttons (10 patients) with maculardystrophy and 8 buttons (8 patients) from enucleatedeyes with chorioideal melanoma (controls) wereanalysed histologically. Immunohistochemical analysiswas performed to investigate the presence of p21, p27,bax, cathepsin and survivin proteins. The number ofpositive cells was determined by analysis of 100 cellsand given in percentages.The bax protein was present in 25.6% of epithelialcells in macular dystrophy corneas but was absent incontrols. P21 and p27 were found in 35.7 and 87.5% ofepithelial cells of macular dystrophy corneas,respectively, but again not in control tissue. In contrast, alower percentage of cathepsin-positive (30.7% vs58.8%) and survivin-positive cells (37.6% vs 52.1%)were present in epithelial cells of macular dystrophycorneas than in control epithelial cells. The differencereached statistical significance in the expression of p21and p27 genes (p<0.05 in both).P21 was positive in 3% of keratocytes, p27 in 1% ofendothelial cells of macular dystrophy corneas butnegative in controls (0%). Bax, cathepsin and survivinimmunopositivity was not detected in keratocytes orendothelial cells of either group. We conclude that the down-regulation of p21, p27and cathepsin in epithelial cells of macular dystrophycorneas may be related to defense mechanisms againstapoptotic cell death.