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Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis
METHODS: The differentially expressed genes (DEGs) were identified using periodontitis-related microarray from the GEO database, and OS-genes were extracted from GeneCards database. The intersection of the OS-genes and the DEGs was considered as oxidative stress-related DEGs (OS-DEGs) in periodontit...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9489423/ https://www.ncbi.nlm.nih.gov/pubmed/36148415 http://dx.doi.org/10.1155/2022/9728172 |
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author | Zhang, Zheng Zheng, Youli Bian, Xiaowei Wang, Minghui Chou, Jiashu Liu, Haifeng Wang, Zuomin |
author_facet | Zhang, Zheng Zheng, Youli Bian, Xiaowei Wang, Minghui Chou, Jiashu Liu, Haifeng Wang, Zuomin |
author_sort | Zhang, Zheng |
collection | PubMed |
description | METHODS: The differentially expressed genes (DEGs) were identified using periodontitis-related microarray from the GEO database, and OS-genes were extracted from GeneCards database. The intersection of the OS-genes and the DEGs was considered as oxidative stress-related DEGs (OS-DEGs) in periodontitis. The Pearson correlation and protein-protein interaction analyses were used to screen key OS-genes. Gene set enrichment, functional enrichment, and pathway enrichment analyses were performed in OS-genes. Based on key OS-genes, a risk score model was constructed through logistic regression, receiver operating characteristic curve, and stratified analyses. RESULTS: In total, 74 OS-DEGs were found in periodontitis, including 65 upregulated genes and 9 downregulated genes. Six of them were identified as key OS-genes (CXCR4, SELL, FCGR3B, FCGR2B, PECAM1, and ITGAL) in periodontitis. All the key OS-genes were significantly upregulated and associated with the increased risk of periodontitis. Functional enrichment analysis showed that these genes were mainly associated with leukocyte cell-cell adhesion, phagocytosis, and cellular extravasation. Pathway analysis revealed that these genes were involved in several signaling pathways, such as leukocyte transendothelial migration and osteoclast differentiation. CONCLUSION: In this study, we screened six key OS-genes that were screened as risk factors of periodontitis. We also identified multiple signaling pathways that might play crucial roles in regulating oxidative stress damage in periodontitis. In the future, more experiments need to be carried out to validate our current findings. |
format | Online Article Text |
id | pubmed-9489423 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-94894232022-09-21 Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis Zhang, Zheng Zheng, Youli Bian, Xiaowei Wang, Minghui Chou, Jiashu Liu, Haifeng Wang, Zuomin Oxid Med Cell Longev Research Article METHODS: The differentially expressed genes (DEGs) were identified using periodontitis-related microarray from the GEO database, and OS-genes were extracted from GeneCards database. The intersection of the OS-genes and the DEGs was considered as oxidative stress-related DEGs (OS-DEGs) in periodontitis. The Pearson correlation and protein-protein interaction analyses were used to screen key OS-genes. Gene set enrichment, functional enrichment, and pathway enrichment analyses were performed in OS-genes. Based on key OS-genes, a risk score model was constructed through logistic regression, receiver operating characteristic curve, and stratified analyses. RESULTS: In total, 74 OS-DEGs were found in periodontitis, including 65 upregulated genes and 9 downregulated genes. Six of them were identified as key OS-genes (CXCR4, SELL, FCGR3B, FCGR2B, PECAM1, and ITGAL) in periodontitis. All the key OS-genes were significantly upregulated and associated with the increased risk of periodontitis. Functional enrichment analysis showed that these genes were mainly associated with leukocyte cell-cell adhesion, phagocytosis, and cellular extravasation. Pathway analysis revealed that these genes were involved in several signaling pathways, such as leukocyte transendothelial migration and osteoclast differentiation. CONCLUSION: In this study, we screened six key OS-genes that were screened as risk factors of periodontitis. We also identified multiple signaling pathways that might play crucial roles in regulating oxidative stress damage in periodontitis. In the future, more experiments need to be carried out to validate our current findings. Hindawi 2022-09-13 /pmc/articles/PMC9489423/ /pubmed/36148415 http://dx.doi.org/10.1155/2022/9728172 Text en Copyright © 2022 Zheng Zhang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zhang, Zheng Zheng, Youli Bian, Xiaowei Wang, Minghui Chou, Jiashu Liu, Haifeng Wang, Zuomin Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis |
title | Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis |
title_full | Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis |
title_fullStr | Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis |
title_full_unstemmed | Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis |
title_short | Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis |
title_sort | identification of key genes and pathways associated with oxidative stress in periodontitis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9489423/ https://www.ncbi.nlm.nih.gov/pubmed/36148415 http://dx.doi.org/10.1155/2022/9728172 |
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