Bioinformatics analysis reveals different gene expression patterns in chondrocytes from knee and finger joints: implications for the effect of mechanical stress in the osteoarthritic development

Abstract

Background Mechanical stress has been well known to be a significant risk factor for the onset and progression of osteoarthritis (OA). The objective of this study is to clarify the key genes and the signaling pathways which is associated with the effect of mechanical stress on OA development. Results A total of 213 Differentially expressed genes (DEGs) were identified in cultured chondrocytes from knee and finger joints, including 101 up- and 112 down-regulated genes, which brought an enrichment in positive or negative regulation of cell proliferation, positive regulation of cell division, positive regulation of apoptotic process and embryonic limb morphogenesis. Two comparison cohorts shared 122 overlapping genes including 49 up- and 73 down-regulated genes, which enriched in DNA replication, cell division, calcium ion binding and positive regulation of apoptotic process. Twelve hub overlapped genes including Cyclin dependent kinase 1 (CDK1), Kinesin family member 11 (KIF11), Mitotic checkpoint serine/threonine kinase (BUB1) and Mitotic arrest deficient 2 like 1 (MAD2L1) were defined and predicted miRNAs of the genes mainly enriched in Transforming growth factor beta (TGF-β) signaling pathway, Wnt signaling pathway and Mitogen activated kinase-like protein (MAPK) signaling pathway. Conclusions Mechanical stress shown multiple influences on chondrocytes, physiologically necessary for maintaining chondrocyte homeostasis and promoting cartilage development, pathologically help for cartilage destruction and OA development via boosting chondrocyte differentiation and hypertrophy and accelerating cell apoptosis.