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Oral Administration of Vitamin D3 Prevents Corneal Damage in a Knock-Out Mouse Model of Sjögren’s Syndrome
Background: Vitamin D deficiency has been associated with dry eye development during Sjögren’s syndrome (SS). Here, we investigated whether repeated oral vitamin D3 supplementation could prevent the corneal epithelium damage in an SS mouse model. Methods: 30 female mouse knock-out for the thrombospo...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9953695/ https://www.ncbi.nlm.nih.gov/pubmed/36831152 http://dx.doi.org/10.3390/biomedicines11020616 |
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author | Trotta, Maria Consiglia Herman, Hildegard Balta, Cornel Rosu, Marcel Ciceu, Alina Mladin, Bianca Gesualdo, Carlo Lepre, Caterina Claudia Russo, Marina Petrillo, Francesco Pieretti, Gorizio Simonelli, Francesca Rossi, Settimio D’Amico, Michele Hermenean, Anca |
author_facet | Trotta, Maria Consiglia Herman, Hildegard Balta, Cornel Rosu, Marcel Ciceu, Alina Mladin, Bianca Gesualdo, Carlo Lepre, Caterina Claudia Russo, Marina Petrillo, Francesco Pieretti, Gorizio Simonelli, Francesca Rossi, Settimio D’Amico, Michele Hermenean, Anca |
author_sort | Trotta, Maria Consiglia |
collection | PubMed |
description | Background: Vitamin D deficiency has been associated with dry eye development during Sjögren’s syndrome (SS). Here, we investigated whether repeated oral vitamin D3 supplementation could prevent the corneal epithelium damage in an SS mouse model. Methods: 30 female mouse knock-out for the thrombospondin 1 gene were randomized (six per group) in untreated mice euthanized at 6 weeks as negative control (C−) or at 12 weeks as the positive control for dry eye (C+). Other mice were sacrificed after 6 weeks of oral vitamin D3 supplementation in the drinking water (1000, 8000, and 20,000 IU/kg/week, respectively). Results: The C+ mice showed alterations in their corneal epithelial morphologies and thicknesses (p < 0.01 vs. C−), while the mice receiving 8000 (M) and 20,000 (H) IU/kg/week of vitamin D3 showed preservation of the corneal epithelium morphology and thickness (p < 0.01 vs. C+). Moreover, while the C+ mice exhibited high levels and activity of corneal tumor necrosis factor alpha converting enzyme (TACE), neovascularization and fibrosis markers; these were all reduced in the M and H mice. Conclusions: Oral vitamin D3 supplementation appeared to counteract the negative effect of TACE on corneal epithelium in a mouse model of SS-associated dry eye. |
format | Online Article Text |
id | pubmed-9953695 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99536952023-02-25 Oral Administration of Vitamin D3 Prevents Corneal Damage in a Knock-Out Mouse Model of Sjögren’s Syndrome Trotta, Maria Consiglia Herman, Hildegard Balta, Cornel Rosu, Marcel Ciceu, Alina Mladin, Bianca Gesualdo, Carlo Lepre, Caterina Claudia Russo, Marina Petrillo, Francesco Pieretti, Gorizio Simonelli, Francesca Rossi, Settimio D’Amico, Michele Hermenean, Anca Biomedicines Article Background: Vitamin D deficiency has been associated with dry eye development during Sjögren’s syndrome (SS). Here, we investigated whether repeated oral vitamin D3 supplementation could prevent the corneal epithelium damage in an SS mouse model. Methods: 30 female mouse knock-out for the thrombospondin 1 gene were randomized (six per group) in untreated mice euthanized at 6 weeks as negative control (C−) or at 12 weeks as the positive control for dry eye (C+). Other mice were sacrificed after 6 weeks of oral vitamin D3 supplementation in the drinking water (1000, 8000, and 20,000 IU/kg/week, respectively). Results: The C+ mice showed alterations in their corneal epithelial morphologies and thicknesses (p < 0.01 vs. C−), while the mice receiving 8000 (M) and 20,000 (H) IU/kg/week of vitamin D3 showed preservation of the corneal epithelium morphology and thickness (p < 0.01 vs. C+). Moreover, while the C+ mice exhibited high levels and activity of corneal tumor necrosis factor alpha converting enzyme (TACE), neovascularization and fibrosis markers; these were all reduced in the M and H mice. Conclusions: Oral vitamin D3 supplementation appeared to counteract the negative effect of TACE on corneal epithelium in a mouse model of SS-associated dry eye. MDPI 2023-02-18 /pmc/articles/PMC9953695/ /pubmed/36831152 http://dx.doi.org/10.3390/biomedicines11020616 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Trotta, Maria Consiglia Herman, Hildegard Balta, Cornel Rosu, Marcel Ciceu, Alina Mladin, Bianca Gesualdo, Carlo Lepre, Caterina Claudia Russo, Marina Petrillo, Francesco Pieretti, Gorizio Simonelli, Francesca Rossi, Settimio D’Amico, Michele Hermenean, Anca Oral Administration of Vitamin D3 Prevents Corneal Damage in a Knock-Out Mouse Model of Sjögren’s Syndrome |
title | Oral Administration of Vitamin D3 Prevents Corneal Damage in a Knock-Out Mouse Model of Sjögren’s Syndrome |
title_full | Oral Administration of Vitamin D3 Prevents Corneal Damage in a Knock-Out Mouse Model of Sjögren’s Syndrome |
title_fullStr | Oral Administration of Vitamin D3 Prevents Corneal Damage in a Knock-Out Mouse Model of Sjögren’s Syndrome |
title_full_unstemmed | Oral Administration of Vitamin D3 Prevents Corneal Damage in a Knock-Out Mouse Model of Sjögren’s Syndrome |
title_short | Oral Administration of Vitamin D3 Prevents Corneal Damage in a Knock-Out Mouse Model of Sjögren’s Syndrome |
title_sort | oral administration of vitamin d3 prevents corneal damage in a knock-out mouse model of sjögren’s syndrome |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9953695/ https://www.ncbi.nlm.nih.gov/pubmed/36831152 http://dx.doi.org/10.3390/biomedicines11020616 |
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