Background
There is little understanding of the molecular processes involved in the pathogenesis of osteoarthritis, limiting early diagnosis and effective treatment of OA. Use of genechips can provide insights into the molecular pathogenesis of diseases. In this study, determination of gene expression profiles of osteoarthritis peripheral blood mononuclear cells will allow exploration of the molecular pathogenesis of OA and find out more candidate biomarkers and potential drug targets of OA. Result: A total of 1231 DEGs were screened out including 791 upregulated DEGs and 440 downregulated DEGs. The most significant upregulated DEG was RPL38, which may inhibit chondrocyte differentiation and synthesis of the extracellular matrix. PIK3CA, PIK3CB, PIK3CD, PIK3R1, MAPK14, IL1A, JUND, FOSL2, and PPP3CA were the gene symbols of the osteoclast differentiation pathway which was the most significant pathway enriched by DEGs. However, the MAPK signaling pathway occupied the core position of all the pathways which can regulate apoptosis, cell cycle, wnt signaling pathway, p53 signaling pathway, and phosphatidylinositol signaling system. Furthermore, PI3Ks may regulate IL1A, JUND, FOSL2 and PPP3CA through the MAPK signaling pathway.
Conclusion
These identified DEGs and pathways may be novel biomarkers to monitor the changes of OA and can be a potential drug target for the treatment of OA.