Han Gong
This BioProject includes spatial transcriptomics data from human osteoarthritis (OA) and normal synovium, as well as RNA-seq data from mouse RAW264.7 cells treated with OPN, to investigate the functional subsets and spatial niches of synovial macrophages. Background: Osteoarthritis (OA) progression is driven by chronic synovitis. However, the spatially organized macrophage subsets that sustain unresolved inflammation through evasion of apoptosis remain poorly characterized. This study investigates the functional subsets and spatial niches of synovial macrophages that regulate apoptotic pathways in OA pathogenesis. Methods: We integrated spatial transcriptomics, scRNA-seq, and in vitro apoptotic models to characterize macrophage interactions in the OA synovium. Results: Spatial multi-omics revealed a TGF-beta-enriched niche in which SPP1+ macrophages expand adjacent to senescent synovial fibroblasts. Distinct from their reported pro-fibrotic roles, SPP1+ macrophages directly suppressed apoptosis of inflammatory macrophages via the SPP1-CD44 signaling axis while recruiting additional myeloid cells through CCL3 secretion. Conclusion: TGF-beta-induced SPP1+ macrophages establish an anti-apoptotic inflammatory niche in OA synovium by directly inhibiting apoptosis of inflammatory macrophages via SPP1 signaling and promoting myeloid recruitment.