International ophthalmology · 2025
Analysis of progranulin concentration in corneal epithelium and tears as a possible biomarker in the clinical diagnosis and progression of keratoconus.
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Akcan Gülben, Özkan Eda Nur Gönültaş, Can Gamze Dereli
Аннотация
PURPOSE: To investigate the expression of progranulin [PGRN] and various inflammatory markers in corneal epithelium and tears of keratoconus [KC] patients and compare them with those of a healthy population.
METHODS: KC patients were allocated to mild, moderate and severe study groups according to Amsler-Krumeich classification. Tear samples for ELISA analysis were collected using plastic capillary tubes from KC patients and healthy individuals. Corneal epithelial tissues were collected from patients who underwent manual epithelial debridement during the epi-off accelerated corneal collagen crosslinking procedure for immunofluorescence. The expression of PGRN, TGF-ß1, MMPs, connexin 43 and TIMP-1 were compared between KC study groups.
RESULTS: The mean tear PRGN levels of the mild [n = 4], moderate [n = 15] and severe [n = 3] KC and healthy [n = 13] groups were 45.94 ± 32.2, 36.63 ± 36.5, 0.52 ± 40.7 and 47.41 ± 47.3 pg/mL, respectively [p = 0.957, p = 0.774 and p = 0.091]. No significant difference was observed between KC study groups regarding tear PGRN levels [p > 0.05]. In immunofluorescence, ImageJ analysis showed that PGRN expression decreased as the KC stage increased. The decrease between KC study groups was found to be statistically significant [p < 0.01]. In contrast to PGRN, a statistically significant increase in TGF-ß1, MMP-1 and TIMP-1 expressions and in similar to PGRN, a statistically significant decrease in MMP-2, MMP-9 and connexin 43 expressions were observed as the KC stage increased.
CONCLUSION: In this study, our findings revealed that PGRN may have a role in the etiopathogenesis of KC. Further studies are needed to support our result.
METHODS: KC patients were allocated to mild, moderate and severe study groups according to Amsler-Krumeich classification. Tear samples for ELISA analysis were collected using plastic capillary tubes from KC patients and healthy individuals. Corneal epithelial tissues were collected from patients who underwent manual epithelial debridement during the epi-off accelerated corneal collagen crosslinking procedure for immunofluorescence. The expression of PGRN, TGF-ß1, MMPs, connexin 43 and TIMP-1 were compared between KC study groups.
RESULTS: The mean tear PRGN levels of the mild [n = 4], moderate [n = 15] and severe [n = 3] KC and healthy [n = 13] groups were 45.94 ± 32.2, 36.63 ± 36.5, 0.52 ± 40.7 and 47.41 ± 47.3 pg/mL, respectively [p = 0.957, p = 0.774 and p = 0.091]. No significant difference was observed between KC study groups regarding tear PGRN levels [p > 0.05]. In immunofluorescence, ImageJ analysis showed that PGRN expression decreased as the KC stage increased. The decrease between KC study groups was found to be statistically significant [p < 0.01]. In contrast to PGRN, a statistically significant increase in TGF-ß1, MMP-1 and TIMP-1 expressions and in similar to PGRN, a statistically significant decrease in MMP-2, MMP-9 and connexin 43 expressions were observed as the KC stage increased.
CONCLUSION: In this study, our findings revealed that PGRN may have a role in the etiopathogenesis of KC. Further studies are needed to support our result.