Bioinformatics analysis of differentially expressed genes in subchondral bone in early experimental osteoarthritis using microarray data

Abstract

Background: Osteoarthritis (OA) is the most common arthritic disease in humans, affecting the majority of individuals over 65 years of age. The aim of this study is to identify the gene expression profile specific to subchondral bone in OA by comparing the different expression profiles in experimental and sham-operation groups. Methods: Gene expression profile GSE30322 was downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were obtained by limma package. And Database for Annotation, Visualization and Integrated Discovery (DAVID) databases were further used to identify the potential gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Furthermore, a protein-protein interaction (PPI) network was constructed and significant modules were extracted. Results: Totally, 588 DEGs were identified including 199 upregulated DEGs and 389 downregulated DEGs screened in OA and sham-operation. GO showed that DEGs were significantly enhanced for ribosomal subunit export from nucleus and molting cycle. KEGG pathway analysis revealed that target genes were enriched in thiamine metabolism. Conclusion: These key candidate DEGs that affect the progression of OA, and these genes might serve as potential therapeutic targets for OA.

Cross-Tissue Analysis Using Machine Learning to Identify Novel Biomarkers for Knee Osteoarthritis

“…Through immune infiltration analysis of synovial gene data, it was found that COL3A1 and MMP9 can be used as potential biomarkers of OA, as confirmed by qRT-PCR and western blot analysis [ 10 ]. Wang et al identified 12 cores of differentially expressed genes (DEGs) through the analysis of gene expression data of the subchondral bone in KOA model mice [ 11 ]. An analysis of gene expression data of the KOA cartilage showed that the difference in BLNK between the OA and normal cartilage groups was most significant, and silencing BLNK was found to inhibit activation of the NF- κ B pathway, thereby inhibiting chondrocyte apoptosis, inflammation, and extracellular matrix degradation [ 12 ].…”