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

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-methylxanthi...

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Autores principales: Cristaldi, Martina, Olivieri, Melania, Pezzino, Salvatore, Spampinato, Giorgia, Lupo, Gabriella, Anfuso, Carmelina Daniela, Rusciano, Dario
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7236597/
https://www.ncbi.nlm.nih.gov/pubmed/32260532
http://dx.doi.org/10.3390/biomedicines8040078
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author Cristaldi, Martina
Olivieri, Melania
Pezzino, Salvatore
Spampinato, Giorgia
Lupo, Gabriella
Anfuso, Carmelina Daniela
Rusciano, Dario
author_facet Cristaldi, Martina
Olivieri, Melania
Pezzino, Salvatore
Spampinato, Giorgia
Lupo, Gabriella
Anfuso, Carmelina Daniela
Rusciano, Dario
author_sort Cristaldi, Martina
collection PubMed
description 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.
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spelling pubmed-72365972020-05-28 Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum Cristaldi, Martina Olivieri, Melania Pezzino, Salvatore Spampinato, Giorgia Lupo, Gabriella Anfuso, Carmelina Daniela Rusciano, Dario Biomedicines Article 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. MDPI 2020-04-05 /pmc/articles/PMC7236597/ /pubmed/32260532 http://dx.doi.org/10.3390/biomedicines8040078 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Cristaldi, Martina
Olivieri, Melania
Pezzino, Salvatore
Spampinato, Giorgia
Lupo, Gabriella
Anfuso, Carmelina Daniela
Rusciano, Dario
Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum
title Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum
title_full Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum
title_fullStr Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum
title_full_unstemmed Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum
title_short Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum
title_sort atropine differentially modulates ecm production by ocular fibroblasts, and its ocular surface toxicity is blunted by colostrum
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7236597/
https://www.ncbi.nlm.nih.gov/pubmed/32260532
http://dx.doi.org/10.3390/biomedicines8040078
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