Fig. 3: OSCAR regulates OA pathogenesis via TRAIL-induced articular chondrocyte apoptosis.

a Selection of putative Oscar targets involved in OA pathogenesis. Venn diagram indicating the number of genes attenuated in articular cartilage Oscar^−/− mice after DMM surgery (left). Hypergeometric p value measuring the significance of enrichment is depicted. Gene-wise scaled gene expression patterns of 1270 common genes in each sample are shown (right). b Functional annotations significantly enriched for 1270 common genes. Hypergeometric tests were performed using the hallmark gene annotation in MsigDB, yielding enrichment scores, defined as −log₁₀ (FDR). c Simplified apoptotic signaling pathway altered by Oscar deficiency. Each gene is colored with the DIF score, defined as the extent to which gene expression is altered by Oscar deficiency. A negative DIF indicates transcriptional suppression in Oscar^−/− mice. The network was visualized by Cytoscape v3.7 software. d, e qRT-PCR (d) and IHC (e) analyses of TRAIL in OA articular cartilage from DMM surgery mice compared to sham-operated mice. Scale bar = 50 μm. f, g mRNA levels (f) and immunostaining (g) for OPG in articular cartilage tissue from sham surgery or DMM surgery mice. Scale bar = 50 μm. h, i Apoptotic articular chondrocytes were detected and quantified by TUNEL assay. Scale bar = 25 μm. Error bars represent mean ± S.E.M. of n = 10 mice (d–g, i). Two-way ANOVA was performed followed by Sidak’s Multiple Comparison’s test, with p values indicated in figure.