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CHAC1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity

Alopecia Areata (AA) is characterised by an autoimmune response to hair follicles (HFs) and its exact pathobiology remains unclear. The current study aims to look into the molecular changes in the skin of AA patients as well as the potential underlying molecular mechanisms of AA in order to identify...

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Autores principales: Karami, Hassan, Nomiri, Samira, Ghasemigol, Mohammad, Mehrvarzian, Niloufar, Derakhshani, Afshin, Fereidouni, Mohammad, Mirimoghaddam, Masoud, Safarpour, Hossein
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9469792/
https://www.ncbi.nlm.nih.gov/pubmed/35983595
http://dx.doi.org/10.1049/syb2.12048
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author Karami, Hassan
Nomiri, Samira
Ghasemigol, Mohammad
Mehrvarzian, Niloufar
Derakhshani, Afshin
Fereidouni, Mohammad
Mirimoghaddam, Masoud
Safarpour, Hossein
author_facet Karami, Hassan
Nomiri, Samira
Ghasemigol, Mohammad
Mehrvarzian, Niloufar
Derakhshani, Afshin
Fereidouni, Mohammad
Mirimoghaddam, Masoud
Safarpour, Hossein
author_sort Karami, Hassan
collection PubMed
description Alopecia Areata (AA) is characterised by an autoimmune response to hair follicles (HFs) and its exact pathobiology remains unclear. The current study aims to look into the molecular changes in the skin of AA patients as well as the potential underlying molecular mechanisms of AA in order to identify potential candidates for early detection and treatment of AA. We applied Weighted Gene Co‐expression Network Analysis (WGCNA) to identify key modules, hub genes, and mRNA–miRNA regulatory networks associated with AA. Furthermore, Chi2 as a machine‐learning algorithm was used to compute the gene importance in AA. Finally, drug‐target construction revealed the potential of repositioning drugs for the treatment of AA. Our analysis using four AA data sets established a network strongly correlated to AA pathogenicity based on GZMA, OXCT2, HOXC13, KRT40, COMP, CHAC1, and KRT83 hub genes. Interestingly, machine learning introduced these genes as important in AA pathogenicity. Besides that, using another ten data sets, we showed that CHAC1 could clearly distinguish AA from similar clinical phenotypes, such as scarring alopecia due to psoriasis. Also, two FDA‐approved drug candidates and 30 experimentally validated miRNAs were identified that affected the co‐expression network. Using transcriptome analysis, suggested CHAC1 as a potential diagnostic predictor to diagnose AA.
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spelling pubmed-94697922022-09-27 CHAC1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity Karami, Hassan Nomiri, Samira Ghasemigol, Mohammad Mehrvarzian, Niloufar Derakhshani, Afshin Fereidouni, Mohammad Mirimoghaddam, Masoud Safarpour, Hossein IET Syst Biol Original Research Alopecia Areata (AA) is characterised by an autoimmune response to hair follicles (HFs) and its exact pathobiology remains unclear. The current study aims to look into the molecular changes in the skin of AA patients as well as the potential underlying molecular mechanisms of AA in order to identify potential candidates for early detection and treatment of AA. We applied Weighted Gene Co‐expression Network Analysis (WGCNA) to identify key modules, hub genes, and mRNA–miRNA regulatory networks associated with AA. Furthermore, Chi2 as a machine‐learning algorithm was used to compute the gene importance in AA. Finally, drug‐target construction revealed the potential of repositioning drugs for the treatment of AA. Our analysis using four AA data sets established a network strongly correlated to AA pathogenicity based on GZMA, OXCT2, HOXC13, KRT40, COMP, CHAC1, and KRT83 hub genes. Interestingly, machine learning introduced these genes as important in AA pathogenicity. Besides that, using another ten data sets, we showed that CHAC1 could clearly distinguish AA from similar clinical phenotypes, such as scarring alopecia due to psoriasis. Also, two FDA‐approved drug candidates and 30 experimentally validated miRNAs were identified that affected the co‐expression network. Using transcriptome analysis, suggested CHAC1 as a potential diagnostic predictor to diagnose AA. John Wiley and Sons Inc. 2022-08-18 /pmc/articles/PMC9469792/ /pubmed/35983595 http://dx.doi.org/10.1049/syb2.12048 Text en © 2022 The Authors. IET Systems Biology published by John Wiley & Sons Ltd on behalf of The Institution of Engineering and Technology. 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 Research
Karami, Hassan
Nomiri, Samira
Ghasemigol, Mohammad
Mehrvarzian, Niloufar
Derakhshani, Afshin
Fereidouni, Mohammad
Mirimoghaddam, Masoud
Safarpour, Hossein
CHAC1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity
title CHAC1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity
title_full CHAC1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity
title_fullStr CHAC1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity
title_full_unstemmed CHAC1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity
title_short CHAC1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity
title_sort chac1 as a novel biomarker for distinguishing alopecia from other dermatological diseases and determining its severity
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9469792/
https://www.ncbi.nlm.nih.gov/pubmed/35983595
http://dx.doi.org/10.1049/syb2.12048
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