Publication: Cell proliferation and apoptosis in stromal corneal dystrophies
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Date
2007
Authors
Szentmáry, N. ; Takács, L. ; Berta, Andras ; Szende, B. ; Süveges, I. ; Módis, L.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
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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