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

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.

Diabetes mellitus promotes susceptibility to periodontitis—novel insight into the molecular mechanisms

“…Consistent with the effect of OS on diabetes, OS in periodontal tissue can also promote the release of proinflammatory factors and activate the NF-κB signal pathway ( 221 , 222 ). ROS exerts antimicrobial activities by exacerbating nucleic acid damage, protein misfolding, lipid peroxidation, and endoplasmic reticulum stress, or mitochondria stress, thereby accelerating autophagy and apoptosis of defective cells ( 223 ).…”

Identification the Low Oxidative Stress Subtype of Periodontitis

“…Many studies have proved that periodontitis is initiated by uncontrolled inflammatory response, and elevated OS plays a vital role in periodontitis by increasing periodontal microenvironmental inflammation. 12 , 25 That means that conventional treatment for periodontitis that focus on combating bacterial pathogens appear to be insufficient, and providing additional antioxidants, such as resveratrol—which react with ROS stoichiometrically—has emerged as a promising treatment for periodontitis. 9 , 26 But recently, studies have shown that the variable therapeutic effect of antioxidants in patients with periodontitis.…”

Knocking Out the Transcription Factor OsNAC092 Promoted Rice Drought Tolerance

“…In addition to participating in the glutathione-ascorbic acid cycle, glutathione can also reduce other types of peroxides, such as membranous peroxides, glyoxal, and herbicides, through GPX [ 18 ]. In addition, GSH can not only directly scavenge ROS accumulated in plants under adverse environments, but it also activates multiple downstream defense systems to indirectly protect cells from damage [ 15 , 49 , 50 ]. For example, GSH can interact with the redox molecules thioredoxin and glutaredoxin, and the plant hormones acetylsalicylic acid and abscisic acid, to regulate gene expression and protein activity [ 51 ].…”