Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis

Author:

Zhang Zheng123ORCID,Zheng Youli4,Bian Xiaowei4,Wang Minghui4,Chou Jiashu1,Liu Haifeng13ORCID,Wang Zuomin5ORCID

Affiliation:

1. Tianjin Stomatological Hospital, School of Medicine, Nankai University, Tianjin 300000, China

2. State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China

3. Tianjin Key Laboratory of Oral and Maxillofacial Function Reconstruction, Tianjin 300041, China

4. The School and Hospital of Stomatology, Tianjin Medical University, Tianjin 300070, China

5. Department of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China

Abstract

Background and Objective. Oxidative stress has been associated with the progression of periodontitis. However, oxidative stress-related genes (OS-genes) have not been used as disease-specific biomarkers that correlate with periodontitis progression. This study is aimed at screening the key OS-genes and pathways in periodontitis by bioinformatics methods. 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.

Funder

Science and Technology Foundation of Tianjin Health Commission

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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