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1,25(OH) (2)D(3) blocks IFNβ production through regulating STING in epithelial layer of oral lichen planus
Stimulator of interferon genes (STING) is reported to exert vital functions in inflammatory responses and autoimmune diseases. Nevertheless, the status and roles of STING in oral lichen planus (OLP) remain elusive. Here, we state that STING and its downstream cytokine interferon‐β (IFNβ) expression...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9258715/ https://www.ncbi.nlm.nih.gov/pubmed/35644988 http://dx.doi.org/10.1111/jcmm.17409 |
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author | Ge, Xuejun Wang, Yaxian Xie, Hanting Li, Ran Zhang, Fang Zhao, Bin Du, Jie |
author_facet | Ge, Xuejun Wang, Yaxian Xie, Hanting Li, Ran Zhang, Fang Zhao, Bin Du, Jie |
author_sort | Ge, Xuejun |
collection | PubMed |
description | Stimulator of interferon genes (STING) is reported to exert vital functions in inflammatory responses and autoimmune diseases. Nevertheless, the status and roles of STING in oral lichen planus (OLP) remain elusive. Here, we state that STING and its downstream cytokine interferon‐β (IFNβ) expression is boosted in the oral keratinocytes from patients suffering OLP in comparison with those from healthy participants. Mechanistically, transcription factor GATA‐binding protein 1 (GATA1) which is highly increased in diseased samples specifically interacts with its element in the promoter of STING to enhance STING transcripts. 1,25(OH)(2)D(3), the active form of vitamin D, is capable of restricting STING and IFNβ increases in oral keratinocyte models resembling OLP in vitro. Moreover, there is a negative correlation between vitamin D receptor (VDR) and STING or IFNβ in human samples. Using plasmids and small interfering RNA transfection technologies, we find 1,25(OH)(2)D(3) regulates STING and IFNβ through a mechanism controlled by the hypoxia‐inducible factor‐1α (HIF‐1α)‐GATA1 axis. Collectively, our findings unveil that 1,25(OH)(2)D(3) lowers STING and IFNβ overexpression in the context of OLP. |
format | Online Article Text |
id | pubmed-9258715 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-92587152022-07-11 1,25(OH) (2)D(3) blocks IFNβ production through regulating STING in epithelial layer of oral lichen planus Ge, Xuejun Wang, Yaxian Xie, Hanting Li, Ran Zhang, Fang Zhao, Bin Du, Jie J Cell Mol Med Original Articles Stimulator of interferon genes (STING) is reported to exert vital functions in inflammatory responses and autoimmune diseases. Nevertheless, the status and roles of STING in oral lichen planus (OLP) remain elusive. Here, we state that STING and its downstream cytokine interferon‐β (IFNβ) expression is boosted in the oral keratinocytes from patients suffering OLP in comparison with those from healthy participants. Mechanistically, transcription factor GATA‐binding protein 1 (GATA1) which is highly increased in diseased samples specifically interacts with its element in the promoter of STING to enhance STING transcripts. 1,25(OH)(2)D(3), the active form of vitamin D, is capable of restricting STING and IFNβ increases in oral keratinocyte models resembling OLP in vitro. Moreover, there is a negative correlation between vitamin D receptor (VDR) and STING or IFNβ in human samples. Using plasmids and small interfering RNA transfection technologies, we find 1,25(OH)(2)D(3) regulates STING and IFNβ through a mechanism controlled by the hypoxia‐inducible factor‐1α (HIF‐1α)‐GATA1 axis. Collectively, our findings unveil that 1,25(OH)(2)D(3) lowers STING and IFNβ overexpression in the context of OLP. John Wiley and Sons Inc. 2022-05-29 2022-07 /pmc/articles/PMC9258715/ /pubmed/35644988 http://dx.doi.org/10.1111/jcmm.17409 Text en © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Ge, Xuejun Wang, Yaxian Xie, Hanting Li, Ran Zhang, Fang Zhao, Bin Du, Jie 1,25(OH) (2)D(3) blocks IFNβ production through regulating STING in epithelial layer of oral lichen planus |
title | 1,25(OH)
(2)D(3)
blocks IFNβ production through regulating STING in epithelial layer of oral lichen planus |
title_full | 1,25(OH)
(2)D(3)
blocks IFNβ production through regulating STING in epithelial layer of oral lichen planus |
title_fullStr | 1,25(OH)
(2)D(3)
blocks IFNβ production through regulating STING in epithelial layer of oral lichen planus |
title_full_unstemmed | 1,25(OH)
(2)D(3)
blocks IFNβ production through regulating STING in epithelial layer of oral lichen planus |
title_short | 1,25(OH)
(2)D(3)
blocks IFNβ production through regulating STING in epithelial layer of oral lichen planus |
title_sort | 1,25(oh)
(2)d(3)
blocks ifnβ production through regulating sting in epithelial layer of oral lichen planus |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9258715/ https://www.ncbi.nlm.nih.gov/pubmed/35644988 http://dx.doi.org/10.1111/jcmm.17409 |
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