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Vitamin-D3 (α-1, 25(OH) 2D3) Protects Retinal Pigment Epithelium From Hyperoxic Insults
PURPOSE: Oxidative stress affects the retinal pigment epithelium (RPE) leading to development of vascular eye diseases. Cholecalciferol (VIT-D) is a known modulator of oxidative stress and angiogenesis. This in vitro study was carried out to evaluate the protective role of VIT-D on RPE cells incubat...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Association for Research in Vision and Ophthalmology
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7325624/ https://www.ncbi.nlm.nih.gov/pubmed/32031576 http://dx.doi.org/10.1167/iovs.61.2.4 |
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author | Murugeswari, Ponnalagu Firoz, Arman Murali, Subramani Vinekar, Anand Krishna, Lekshmi Anandula, Venkata Ramana Jeyabalan, Nallathambi Chevour, Priyanka Jayadev, Chaitra Shetty, Rohit Carpentier, Gilles Kumaramanickavel, Govindaswamy Ghosh, Arkasubhra Das, Debashish |
author_facet | Murugeswari, Ponnalagu Firoz, Arman Murali, Subramani Vinekar, Anand Krishna, Lekshmi Anandula, Venkata Ramana Jeyabalan, Nallathambi Chevour, Priyanka Jayadev, Chaitra Shetty, Rohit Carpentier, Gilles Kumaramanickavel, Govindaswamy Ghosh, Arkasubhra Das, Debashish |
author_sort | Murugeswari, Ponnalagu |
collection | PubMed |
description | PURPOSE: Oxidative stress affects the retinal pigment epithelium (RPE) leading to development of vascular eye diseases. Cholecalciferol (VIT-D) is a known modulator of oxidative stress and angiogenesis. This in vitro study was carried out to evaluate the protective role of VIT-D on RPE cells incubated under hyperoxic conditions. METHODS: Cadaver primary RPE (PRPE) cells were cultured in hyperoxia (40% O(2)) with or without VIT-D (α-1, 25(OH) 2D3). The functional and physiological effects of PRPE cells with VIT-D treatment were analyzed using molecular and biochemical tools. RESULTS: Vascular signaling modulators, such as vascular endothelial growth factor (VEGF) and Notch, were reduced in hyperoxic conditions but significantly upregulated in the presence of VIT-D. Additionally, PRPE conditioned medium with VIT-D induced the tubulogenesis in primary human umbilical vein endothelial cells (HUVEC) cells. VIT-D supplementation restored phagocytosis and transmembrane potential in PRPE cells cultured under hyperoxia. CONCLUSIONS: VIT-D protects RPE cells and promotes angiogenesis under hyperoxic insult. These findings may give impetus to the potential of VIT-D as a therapeutic agent in hyperoxia induced retinal vascular diseases. |
format | Online Article Text |
id | pubmed-7325624 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | The Association for Research in Vision and Ophthalmology |
record_format | MEDLINE/PubMed |
spelling | pubmed-73256242020-07-07 Vitamin-D3 (α-1, 25(OH) 2D3) Protects Retinal Pigment Epithelium From Hyperoxic Insults Murugeswari, Ponnalagu Firoz, Arman Murali, Subramani Vinekar, Anand Krishna, Lekshmi Anandula, Venkata Ramana Jeyabalan, Nallathambi Chevour, Priyanka Jayadev, Chaitra Shetty, Rohit Carpentier, Gilles Kumaramanickavel, Govindaswamy Ghosh, Arkasubhra Das, Debashish Invest Ophthalmol Vis Sci Biochemistry and Molecular Biology PURPOSE: Oxidative stress affects the retinal pigment epithelium (RPE) leading to development of vascular eye diseases. Cholecalciferol (VIT-D) is a known modulator of oxidative stress and angiogenesis. This in vitro study was carried out to evaluate the protective role of VIT-D on RPE cells incubated under hyperoxic conditions. METHODS: Cadaver primary RPE (PRPE) cells were cultured in hyperoxia (40% O(2)) with or without VIT-D (α-1, 25(OH) 2D3). The functional and physiological effects of PRPE cells with VIT-D treatment were analyzed using molecular and biochemical tools. RESULTS: Vascular signaling modulators, such as vascular endothelial growth factor (VEGF) and Notch, were reduced in hyperoxic conditions but significantly upregulated in the presence of VIT-D. Additionally, PRPE conditioned medium with VIT-D induced the tubulogenesis in primary human umbilical vein endothelial cells (HUVEC) cells. VIT-D supplementation restored phagocytosis and transmembrane potential in PRPE cells cultured under hyperoxia. CONCLUSIONS: VIT-D protects RPE cells and promotes angiogenesis under hyperoxic insult. These findings may give impetus to the potential of VIT-D as a therapeutic agent in hyperoxia induced retinal vascular diseases. The Association for Research in Vision and Ophthalmology 2020-02-07 2020-02 /pmc/articles/PMC7325624/ /pubmed/32031576 http://dx.doi.org/10.1167/iovs.61.2.4 Text en Copyright 2020 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. |
spellingShingle | Biochemistry and Molecular Biology Murugeswari, Ponnalagu Firoz, Arman Murali, Subramani Vinekar, Anand Krishna, Lekshmi Anandula, Venkata Ramana Jeyabalan, Nallathambi Chevour, Priyanka Jayadev, Chaitra Shetty, Rohit Carpentier, Gilles Kumaramanickavel, Govindaswamy Ghosh, Arkasubhra Das, Debashish Vitamin-D3 (α-1, 25(OH) 2D3) Protects Retinal Pigment Epithelium From Hyperoxic Insults |
title | Vitamin-D3 (α-1, 25(OH) 2D3) Protects Retinal Pigment Epithelium From Hyperoxic Insults |
title_full | Vitamin-D3 (α-1, 25(OH) 2D3) Protects Retinal Pigment Epithelium From Hyperoxic Insults |
title_fullStr | Vitamin-D3 (α-1, 25(OH) 2D3) Protects Retinal Pigment Epithelium From Hyperoxic Insults |
title_full_unstemmed | Vitamin-D3 (α-1, 25(OH) 2D3) Protects Retinal Pigment Epithelium From Hyperoxic Insults |
title_short | Vitamin-D3 (α-1, 25(OH) 2D3) Protects Retinal Pigment Epithelium From Hyperoxic Insults |
title_sort | vitamin-d3 (α-1, 25(oh) 2d3) protects retinal pigment epithelium from hyperoxic insults |
topic | Biochemistry and Molecular Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7325624/ https://www.ncbi.nlm.nih.gov/pubmed/32031576 http://dx.doi.org/10.1167/iovs.61.2.4 |
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