RNA‐seq analysis reveals different gene ontologies and pathways in rheumatoid arthritis and Kashin–Beck disease

Abstract Aims To understand the pathogenesis of cartilage damage in Kashin–Beck disease ( KBD ) and rheumatoid arthritis ( RA ) which similar clinical symptoms. Methods RNA sequencing ( RAN ‐seq) analysis was used to reveal the different pathogeneses between KBD and RA . The messenger RNA expression profiles of articular cartilage isolated from KBD patients (n = 3) and RA patients (n = 3) were compared using RNA ‐seq analysis. Differentially expressed genes ( DEG s) were determined using the Benjamini–Hochberg approach. The Database for Annotation, Visualization and Integrated Discovery ( DAVID 6.7) was employed to assess functional categories and Gene Ontology ( GO ). The Kyoto Encyclopedia of Genes and Genomes ( KEGG ) Orthology Based Annotation System ( KOBAS 2.0) was used to identify significantly enriched KEGG pathways. Results In the individually sequenced dataset, we identified 1568 significant DEG s in KBD compared to RA (232 up‐regulated genes and 1336 down‐regulated genes). GO function analysis identified nine significant biological processes ( BP s), eight molecular functions ( MF s), and five cell components ( CC s) in KBD , and also the top ten ranked significant BP s, MF s and CC s were found in RA . The KEGG pathway enrichment analysis identified biosynthesis of amino acids involved in KBD . The chemokine signaling pathway, nuclear factor‐kappa B signaling pathway, B cell receptor signaling pathway, leukocyte transendothelial migration, and osteoclast differentiation were involved in RA . Conclusions RNA ‐seq revealed that proteoglycan‐mediated metabolic disorders contributed to the onset of KBD , whereas immune dysregulation was apparently involved in the pathogenesis of RA .