Importance of gene signatures for rheumatoid arthritis and osteoarthritis based on bioinformatics analysis
Rheumatoid arthritis (RA) is a persistant inflammatory problem which can lead to progressive disability, early mortality and other systemic complications. Osteoarthritis (OA) is the most common joint disease which causes pain, disability and loss of joint function. Both RA and OA are incurable.
A reasearch work was done which was focused on identifying gene signatures during RA and OA and used these to elucidate the underlying modular processes.
In this study, the GSE7669 mRNA expression microarray data was procured from RA and OA synovial fibroblasts (n=6 each) via Gene Expression Omnibus database. The Linear Models for microarray analysis package was used for comparison of OA samples with differentially expressed genes (DEGs) in RA synovial samples. Database for Annotation Visualization and Integrated Discovery was utilized for the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. A protein-protein interaction network was built and modules were further examined using the Molecular Complex Detection plugin of Cytoscape. With the help of contrasting RA and OA synovial samples (96 up and 85 downregulated genes), a total of 181 DEGs were identified. The important DEGs in module 1, comprising collagen, type I, α 1 (COL1A1), COL3A1, COL4A1 and COL11A1, were predominantly enhanced in the extracellular matrix (ECM) receptor interaction and focal adhesion pathways. Also, significant DEGs in module 2, like radical S-adenosyl methionine domain containing 2 (RSAD2), 2'-5'-oligoadenylate synthetase 2 (OAS2), myxovirus (influenza virus) resistance 1 (MX1) and ISG15 ubiquitin-like modifier (ISG15), were predominantly realted to immune function pathways.
Therefore, the current study revealed that RSAD2, OAS2, MX1 and ISG15 may be remarkable gene signatures in RA development via regulation of the immune response. COL3A1, COL4A1, COL1A1 and COL11A1 may be the essential gene signatures in OA development via involvement in the pathways of ECM-receptor interactions and focal adhesions.