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Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid

Keloid is a benign fibro‐proliferative dermal tumour formed by an abnormal scarring response to injury and characterised by excessive collagen accumulation and invasive growth. The pathophysiology of keloids is complex, and the treatment for keloids is still an unmet medical need. Here, we investiga...

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Autores principales: Xu, Hailin, Wang, Zhiyong, Yang, Hao, Zhu, Jiayuan, Hu, Zhicheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10088861/
https://www.ncbi.nlm.nih.gov/pubmed/36517972
http://dx.doi.org/10.1111/iwj.14031
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author Xu, Hailin
Wang, Zhiyong
Yang, Hao
Zhu, Jiayuan
Hu, Zhicheng
author_facet Xu, Hailin
Wang, Zhiyong
Yang, Hao
Zhu, Jiayuan
Hu, Zhicheng
author_sort Xu, Hailin
collection PubMed
description Keloid is a benign fibro‐proliferative dermal tumour formed by an abnormal scarring response to injury and characterised by excessive collagen accumulation and invasive growth. The pathophysiology of keloids is complex, and the treatment for keloids is still an unmet medical need. Here, we investigated the transcriptional gene that influences keloid development by comparing keloid, non‐lesioned keloid skin and normal skin as well as keloid fibroblast and normal fibroblast (GSE83286, GSE92566, GSE44270). Based on the analysis, 146 up‐regulated genes and 48 down‐regulated genes were found in keloid tissue compared with normal skin and keloid no‐lesioned skin. Eleven genes were further identified by overlapping the DEGs from keloid tissue described previously with DEGs in keloid fibroblast. The overlapped genes included PRR16, SFRP2, EDIL3, GERM1, POSTN, PDE3A, GALNT5, F2RL2, EYA4, ZFHX4, and AIM2. POSTN is the most crucial node in PPI network, which mainly correlate to collagen‐related genes. Moreover, siRNA knockdown identified POSTN is a crucial regulatory gene that regulates keloid fibroblast migration and collagen I, collagen III expression level. In conclusion, our study identified 11 hub genes that play crucial role in keloid formation and provided insights for POSTN to be the therapeutic target for keloid through bioinformatic analysis of three datasets. Additionally, our results would support the development of future therapeutic strategies.
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spelling pubmed-100888612023-04-12 Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid Xu, Hailin Wang, Zhiyong Yang, Hao Zhu, Jiayuan Hu, Zhicheng Int Wound J Original Articles Keloid is a benign fibro‐proliferative dermal tumour formed by an abnormal scarring response to injury and characterised by excessive collagen accumulation and invasive growth. The pathophysiology of keloids is complex, and the treatment for keloids is still an unmet medical need. Here, we investigated the transcriptional gene that influences keloid development by comparing keloid, non‐lesioned keloid skin and normal skin as well as keloid fibroblast and normal fibroblast (GSE83286, GSE92566, GSE44270). Based on the analysis, 146 up‐regulated genes and 48 down‐regulated genes were found in keloid tissue compared with normal skin and keloid no‐lesioned skin. Eleven genes were further identified by overlapping the DEGs from keloid tissue described previously with DEGs in keloid fibroblast. The overlapped genes included PRR16, SFRP2, EDIL3, GERM1, POSTN, PDE3A, GALNT5, F2RL2, EYA4, ZFHX4, and AIM2. POSTN is the most crucial node in PPI network, which mainly correlate to collagen‐related genes. Moreover, siRNA knockdown identified POSTN is a crucial regulatory gene that regulates keloid fibroblast migration and collagen I, collagen III expression level. In conclusion, our study identified 11 hub genes that play crucial role in keloid formation and provided insights for POSTN to be the therapeutic target for keloid through bioinformatic analysis of three datasets. Additionally, our results would support the development of future therapeutic strategies. Blackwell Publishing Ltd 2022-12-14 /pmc/articles/PMC10088861/ /pubmed/36517972 http://dx.doi.org/10.1111/iwj.14031 Text en © 2022 The Authors. International Wound Journal published by Medicalhelplines.com Inc (3M) and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Xu, Hailin
Wang, Zhiyong
Yang, Hao
Zhu, Jiayuan
Hu, Zhicheng
Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid
title Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid
title_full Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid
title_fullStr Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid
title_full_unstemmed Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid
title_short Bioinformatics analysis and identification of dysregulated POSTN in the pathogenesis of keloid
title_sort bioinformatics analysis and identification of dysregulated postn in the pathogenesis of keloid
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10088861/
https://www.ncbi.nlm.nih.gov/pubmed/36517972
http://dx.doi.org/10.1111/iwj.14031
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