Objective: Rheumatoid arthritis (RA) is considered to be a chronic immune disease pathologically characterized by synovial inflammation and bone destruction. At present, the potential pathogenesis of RA is still unclear. Hub genes are recognized to play a pivotal role in the occurrence and progression of RA.
Methods: Firstly, we attempted to screen hub genes that are associated with RA, to clarify the underlying pathological mechanisms of RA, and to offer potential treatment methods for RA. We acquired these datasets (GSE12021, GSE55235, and GSE55457) of RA patients and healthy samples from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were recognized via R software. Then, Gene ontology (GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were utilized to deeply explore the underlying biological functions and pathways closely associated with RA. In addition, a protein-protein interaction (PPI) network was built to further evaluate and screen for hub genes. Finally, on the basis of the results of PPI analysis, we confirmed the mRNA expression levels of five hub genes in the synovial tissue of rats modeled with RA.
Results: In the human microarray datasets, LCK, JAK2, SOCS3, STAT1, and EGFR were identified as hub genes associated with RA by bioinformatics analysis. Furthermore, we verified the differential expression levels of hub genes in rat synovial tissues via qRT-PCR (P < 0.05).
Conclusions: Our findings suggest that the hub genes LCK, JAK2, SOCS3, STAT1, and EGFR might have vital roles in the progression of RA and may offer novel therapeutic treatments for RA.
Keywords: Rheumatoid arthritis; bioinformatics; hub gene; protein-protein interaction network; synovial tissue.
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