Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum.

Martina Cristaldi,Gabriella Lupo,Carmelina Daniela Anfuso,Giorgia Spampinato,Melania Olivieri,Dario Rusciano,Salvatore Pezzino

doi:10.3390/biomedicines8040078

Abstract

Background: The etiology and the mechanism behind atropine treatment of progressive myopia are still poorly understood. Our study addressed the role of scleral and choroidal fibroblasts in myopia development and atropine function. Methods: Fibroblasts treated in vitro with atropine or 7-methylxanthine were tested for ECM production by Western blotting. Corneal epithelial cells were treated with atropine in the presence or absence of colostrum or fucosyl-lactose, and cell survival was evaluated by the MTT metabolic test. Results: Atropine and 7-methyl-xanthine stimulated collagen I and fibronectin production in scleral fibroblasts, while they inhibited their production in choroidal fibroblasts. Four days of treatment with atropine of corneal epithelial cells significantly decreased cell viability, which could be prevented by the presence of colostrum or fucosyl-lactose. Conclusions: Our results show that atropine may function in different ways in different eye districts, strengthening the scleral ECM and increasing permeability in the choroid. The finding that colostrum or fucosyl-lactose attenuate the corneal epithelial toxicity after long-term atropine treatment suggests the possibility that both compounds can efficiently blunt its toxicity in children subjected to chronic atropine treatment.

Highlights

Myopia is an aberrometric defect of vision well defined in its anatomy and physiology, its etiology is not completely clarified
Starting from the hypothesis that the elongation of the eye globe in myopia should involve the biosynthesis of extracellular matrix (ECM) proteins in the sclera, and that atropine might interfere with this process, we treated human scleral fibroblast cell line (HSF) cells with increasing doses of atropine for 24 and 48 h, and measured the amount of collagen and fibronectin in cell lysates
What we found and showed in this study is that the effect of atropine on human scleral fibroblasts is to dramatically enhance their type I collagen production, which is in line with the expected efficacy of atropine to slow down myopia progression

Summary

Introduction

Myopia is an aberrometric defect of vision well defined in its anatomy and physiology, its etiology is not completely clarified. Our study addressed the role of scleral and choroidal fibroblasts in myopia development and atropine function. Corneal epithelial cells were treated with atropine in the presence or absence of colostrum or fucosyl-lactose, and cell survival was evaluated by the MTT metabolic test. Four days of treatment with atropine of corneal epithelial cells significantly decreased cell viability, which could be prevented by the presence of colostrum or fucosyl-lactose. Conclusions: Our results show that atropine may function in different ways in different eye districts, strengthening the scleral ECM and increasing permeability in the choroid. The finding that colostrum or fucosyl-lactose attenuate the corneal epithelial toxicity after long-term atropine treatment suggests the possibility that both compounds can efficiently blunt its toxicity in children subjected to chronic atropine treatment

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Discussion

Conclusion