Abstract
BackgroundRheumatoid arthritis (RA) is a common chronic autoimmune disease characterized by inflammation of the synovial membrane. However, the etiology and underlying molecular events of RA are unclear. Here, we applied bioinformatics analysis to identify the key genes involved in RA.MethodsGSE77298 was downloaded from the Gene Expression Omnibus (GEO) database. We used the R software screen the differentially expressed genes (DEGs). Gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway were analyzed by using the DAVID online tool. The STRING database was used to analyze the interaction of differentially encoded proteins. PPI interaction network was divided into subnetworks using MCODE algorithm and was analyzed using Cytoscape. Gene set enrichment analysis (GSEA) was performed to identify relevant biological functions. qRT-PCR analysis was also performed to verify the expression of identified hub DEGs.ResultsA total of 4062 differentially expressed genes were selected, including 1847 upregulated genes and 2215 downregulated genes. In the biological process, DEGs were mainly concentrated in the fields of muscle filament sliding, muscle contraction, intracellular signal transduction, cardiac muscle contraction, signal transduction, and skeletal muscle tissue development. In the cellular components, DEGs were mainly concentrated in the parts of cytosol, Z disk, membrane, extracellular exosome, mitochondrion, and M band. In molecular functions, DEGs were mainly concentrated in protein binding, structural constituent of muscle, actin binding, and actin filament binding. KEGG pathway analysis shows that DEGs mainly focuses on pathways about lysosome, Wnt/β-catenin signaling pathway, and NF-κB signaling pathway. CXCR3, GNB4, and CXCL16 were identified as the core genes that involved in the progression of RA. By qRT-PCR analysis, we found that CXCR3, GNB4, and CXCL16 were significantly upregulated in RA tissue as compared to healthy controls.ConclusionIn conclusion, DEGs and hub genes identified in the present study help us understand the molecular mechanisms underlying the progression of RA, and provide candidate targets for diagnosis and treatment of RA.
Highlights
Rheumatoid arthritis (RA) is a common chronic autoimmune disease characterized by inflammation of the synovial membrane
Hierarchical clustering for sample selection The total samples were analyzed by hierarchical clustering, no samples were with high heterogeneity and eliminated
differentially expressed genes (DEGs) were mainly concentrated in the fields of muscle filament sliding, muscle contraction, intracellular signal transduction, cardiac muscle contraction, signal transduction, skeletal muscle tissue development, sarcomere organization, antigen processing and presentation of peptide antigen via MHC class I, tricarboxylic acid cycle, and regulation of release of sequestered calcium ion into cytosol by sarcoplasmic reticulum (Fig. 4)
Summary
Rheumatoid arthritis (RA) is a common chronic autoimmune disease characterized by inflammation of the synovial membrane. Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation, hyperproliferation of synovial tissue, and progressive destruction of multiple joints [1, 2]. RA mainly targets the synovium of diarthrodial joints [3, 4]. The pathogenesis of RA mainly focuses on autoantibodies and immune complexes [9]. RA involves T cell-mediated antigen-specific response, T cellindependent cytokine network, and aggressive tumorlike behavior of rheumatoid synovium [10]. Significant thickening of the synovium is the most typical pathological change of RA [12]. Studies have shown that synovial inflammation plays an important role in the pathogenesis of RA. The exact pathogenesis of RA is unclear
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