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

被引:11
|
作者
Zhang, Zheng [1 ,2 ,3 ]
Zheng, Youli [4 ]
Bian, Xiaowei [4 ]
Wang, Minghui [4 ]
Chou, Jiashu [1 ]
Liu, Haifeng [1 ,3 ]
Wang, Zuomin [5 ]
机构
[1] Nankai Univ, Tianjin Stomatol Hosp, Sch Med, Tianjin 300000, Peoples R China
[2] Peking Univ, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
[3] Tianjin Key Lab Oral & Maxillofacial Funct Reconst, Tianjin 300041, Peoples R China
[4] Tianjin Med Univ, Sch & Hosp Stomatol, Tianjin 300070, Peoples R China
[5] Capital Med Univ, Beijing Chao Yang Hosp, Dept Stomatol, Beijing 100020, Peoples R China
基金
中国国家自然科学基金;
关键词
EXPRESSION; CELLS;
D O I
10.1155/2022/9728172
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
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页数:27
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