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  • Title: Identification of differentially expressed genes in synovial tissue of rheumatoid arthritis and osteoarthritis in patients.
    Author: Li WC, Bai L, Xu Y, Chen H, Ma R, Hou WB, Xu RJ.
    Journal: J Cell Biochem; 2019 Mar; 120(3):4533-4544. PubMed ID: 30260019.
    Abstract:
    Rheumatoid arthritis (RA) and osteoarthritis (OA) are the common joints disorder in the world. Although they have showed the analogous clinical manifestation and overlapping cellular and molecular foundation, the pathogenesis of RA and OA were different. The pathophysiologic mechanisms of arthritis in RA and OA have not been investigated thoroughly. Thus, the aim of study is to identify the potential crucial genes and pathways associated with RA and OA and further analyze the molecular mechanisms implicated in genesis. First, we compared gene expression profiles in synovial tissue between RA and OA from the National Center of Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database. Gene Expression Series (GSE) 1919, GSE55235, and GSE36700 were downloaded from the GEO database, including 20 patients of OA and 21 patients of RA. Differentially expressed genes (DEGs) including "CXCL13," "CD247," "CCL5," "GZMB," "IGKC," "IL7R," "UBD///GABBR1," "ADAMDEC1," "BTC," "AIM2," "SHANK2," "CCL18," "LAMP3," "CR1," and "IL32." Second, Gene Ontology analyses revealed that DEGs were significantly enriched in integral component of extracellular space, extracellular region, and plasma membrane in the molecular function group. Signaling pathway analyses indicated that DEGs had common pathways in chemokine signaling pathway, cytokine-cytokine receptor interaction, and cytosolic DNA-sensing pathway. Third, DEGs showed the complex DEGs protein-protein interaction network with the Coexpression of 83.22%, Shared protein domains of 8.40%, Colocalization of 4.76%, Predicted of 2.87%, and Genetic interactions of 0.75%. In conclusion, the novel DEGs and pathways between RA and OA identified in this study may provide new insight into the underlying molecular mechanisms of RA.
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