A gene expression analysis and immune infiltration between lesioned and preserved subchondral bone in osteoarthritis
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This study identified 1010 differentially expressed genes between lesioned and preserved subchondral bone in osteoarthritis, pinpointing JUN, TNF, and IL1B as hub genes and observing less adipocyte and endothelial cell infiltration in lesioned areas.
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Abstract
Background Osteoarthritis (OA) is a degenerative disease which need more research. The purpose of this study was to performed gene expression analysis and immune infiltration between lesioned and preserved subchondral bone, and validation with datasets and experiment of multiple tissues. Methods The different expressed genes(DEGs) of GSE51588 datasets between lesioned and preserved tibial plateaus of OA patients were conducted. Moreover, functional annotation and protein–protein interaction (PPI) network were applied for exploring the potential therapeutic targets in OA subchondral bones between lesioned and preserved sides. In addition, multiple tissues were used to screen out co-expressed genes and the expression levels of identified candidate DEGs was detected by quantitative real-time polymerase chain reaction (qRT-PCR) in OA. Finally, immune infiltration analysis was conducted. Results A total of 1010 DEGs were identified, including upregulated 423 genes, 587 downregulated genes. Upregulated genes showed that BP terms were enriched in “skeletal system development”, “sister chromatid cohesion”,”ossification” etc. Pathways were enriched in “Wnt signaling pathway,” “Proteoglycans in cancer,” Downregulated genes showed that BP terms were enriched in “inflammatory response,” “xenobiotic metabolic process”, “positive regulation of inflammatory response”. Pathways were enriched in “Neuroactive ligand–receptor interaction”, “AMPK signaling pathway” etc. JUN, TNF, IL1B,were the hub genes in the PPI network. Col1A1 and LRRC15 were screened out by multiple datasets and validated by experiments. Immune infiltration showed adipocytes and endothelial cells infiltrated less in lesioned samples. Conclusion Our research might provide valuable information for exploring the pathogenesis mechanism of OA and identifying the potential therapy targets for OA diagnosis.
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