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Edoardo Midena, Silvia Bini, Alessandra Micera, Graziana Esposito, Marianna Berton, Raffaele Parrozzani, Elisabetta Pilotto, Stela Vujosevic; Müller Cells Changes in Diabetic Macular Edema: Molecular Biomarkers in Regressing Cases . Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4713. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
To correlate some specific biomarkers of Müller cells activation in diabetic eyes with regressing versus persistent diabetic macular edema (DME).
Twenty-six diabetic eyes with regressing diabetic macular edema (DME) were compared with 26 persistent DME eyes, and 20 diabetic eyes without DME. Aqueous humor was sampled in all eyes using a 30 gauge needle through a peripheral clear cornea approach. Each subject underwent full ophthalmic examination, and SD-OCT retinal layers segmentation, before aqueous humor sampling. Each sample was analyzed to quantify: glial fibrillary acidic protein (GFAP), AQP4 and Kir 4.1 as biomarkers of Müller cells activation, by ELISA. ANOVA analysis followed by Tukey-Kramer post-hoc test was applied.
Mean concentration of GFAP, Kir 4.1 and AQP4 significantly decreased in DME eyes versus non DME eyes (p<0.002, for each comparison). Regressing DME eyes showed a significant increase of Müller cells biomarkers compared to persistent DME eyes (p<0.005), never reaching the values of non DME eyes (p< 0.002). AQP4 and Kir 4.1 better represented Müller cells activity (p< 0.001 and < 0.002, in all comparison).
The activation of Müller cells in diabetic retina has been confirmed by the increase of specific biomarkers, even in the aqueous humor. The decrease of Müller cells specific biomarkers in eyes with DME, associated with cystic changes in the middle retina, is a sign of Müller cells degeneration, as previously reported. This study shows that when DME regresses Müller cells activity may be, at least partially, restored, providing the opportunity for retinal recovery in both metabolic and functional activity. These results show that Müller cells activity is critical in the pathophysiology and management of DME.
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