Gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.

Oral lichen planus (OLP) is one of the most prevalent oral mucosal diseases, but there is no cure for OLP yet. The aim of this study was to gain insights into the role of barrier dysfunction and infection in OLP pathogenesis through analysis of transcriptome datasets available in public databases. T...

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Autores principales: Phuc Thi-Duy Vo, Sun Shim Choi, Hae Ryoun Park, Ahreum Lee, Sung-Hee Jeong, Youngnim Choi
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Publicado: Public Library of Science (PLoS) 2021
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spelling oai:doaj.org-article:025be30dc4cc437cb4251c10a8a974492021-12-02T20:06:19ZGene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.1932-620310.1371/journal.pone.0257356https://doaj.org/article/025be30dc4cc437cb4251c10a8a974492021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0257356https://doaj.org/toc/1932-6203Oral lichen planus (OLP) is one of the most prevalent oral mucosal diseases, but there is no cure for OLP yet. The aim of this study was to gain insights into the role of barrier dysfunction and infection in OLP pathogenesis through analysis of transcriptome datasets available in public databases. Two transcriptome datasets were downloaded from the Gene Expression Omnibus database and analyzed as whole and as partial sets after removing outliers. Differentially expressed genes (DEGs) upregulated in the dataset of OLP versus healthy epithelium were significantly enriched in epidermal development, keratinocyte differentiation, keratinization, responses to bacterial infection, and innate immune response. In contrast, the upregulated DEGs in the dataset of the mucosa predominantly reflected chemotaxis of immune cells and inflammatory/immune responses. Forty-three DEGs overlapping in the two datasets were identified after removing outliers from each dataset. The overlapping DEGs included genes associated with hyperkeratosis (upregulated LCE3E and TMEM45A), wound healing (upregulated KRT17, IL36G, TNC, and TGFBI), barrier defects (downregulated FRAS1 and BCL11A), and response to infection (upregulated IL36G, ADAP2, DFNA5, RFTN1, LITAF, and TMEM173). Immunohistochemical examination of IL-36γ, a protein encoded by one of the DEGs IL36G, in control (n = 7) and OLP (n = 25) tissues confirmed the increased expression of IL-36γ in OLP. Collectively, we identified gene signatures associated with hyperkeratosis, wound healing, barrier defects, and response to infection in OLP. IL-36γ, a cytokine involved in both wound repair and antimicrobial defense, may be a possible therapeutic target in OLP.Phuc Thi-Duy VoSun Shim ChoiHae Ryoun ParkAhreum LeeSung-Hee JeongYoungnim ChoiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 9, p e0257356 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Phuc Thi-Duy Vo
Sun Shim Choi
Hae Ryoun Park
Ahreum Lee
Sung-Hee Jeong
Youngnim Choi
Gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.
description Oral lichen planus (OLP) is one of the most prevalent oral mucosal diseases, but there is no cure for OLP yet. The aim of this study was to gain insights into the role of barrier dysfunction and infection in OLP pathogenesis through analysis of transcriptome datasets available in public databases. Two transcriptome datasets were downloaded from the Gene Expression Omnibus database and analyzed as whole and as partial sets after removing outliers. Differentially expressed genes (DEGs) upregulated in the dataset of OLP versus healthy epithelium were significantly enriched in epidermal development, keratinocyte differentiation, keratinization, responses to bacterial infection, and innate immune response. In contrast, the upregulated DEGs in the dataset of the mucosa predominantly reflected chemotaxis of immune cells and inflammatory/immune responses. Forty-three DEGs overlapping in the two datasets were identified after removing outliers from each dataset. The overlapping DEGs included genes associated with hyperkeratosis (upregulated LCE3E and TMEM45A), wound healing (upregulated KRT17, IL36G, TNC, and TGFBI), barrier defects (downregulated FRAS1 and BCL11A), and response to infection (upregulated IL36G, ADAP2, DFNA5, RFTN1, LITAF, and TMEM173). Immunohistochemical examination of IL-36γ, a protein encoded by one of the DEGs IL36G, in control (n = 7) and OLP (n = 25) tissues confirmed the increased expression of IL-36γ in OLP. Collectively, we identified gene signatures associated with hyperkeratosis, wound healing, barrier defects, and response to infection in OLP. IL-36γ, a cytokine involved in both wound repair and antimicrobial defense, may be a possible therapeutic target in OLP.
format article
author Phuc Thi-Duy Vo
Sun Shim Choi
Hae Ryoun Park
Ahreum Lee
Sung-Hee Jeong
Youngnim Choi
author_facet Phuc Thi-Duy Vo
Sun Shim Choi
Hae Ryoun Park
Ahreum Lee
Sung-Hee Jeong
Youngnim Choi
author_sort Phuc Thi-Duy Vo
title Gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.
title_short Gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.
title_full Gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.
title_fullStr Gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.
title_full_unstemmed Gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.
title_sort gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.
publisher Public Library of Science (PLoS)
publishDate 2021
url https://doaj.org/article/025be30dc4cc437cb4251c10a8a97449
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