ArticleCell death & disease2022
Pentraxin 3 regulated by miR-224-5p modulates macrophage reprogramming and exacerbates osteoarthritis associated synovitis by targeting CD32.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Spatial multi‑omics identifies an SPP1+ macrophage‑driven anti‑apoptotic niche in osteoarthritis synovium via the SPP1‑CD44 axis.International journal of molecular medicine · 2026Article
- Integrated hydrogel system targeting AMPK/PPARγ signaling in osteoarthritis immunometabolic regulation.Journal of nanobiotechnology · 2026Article
- 3D-bioprinted adipose-derived stem cell-secreted GAS6Journal of nanobiotechnology · 2026Article
- Immuno-based profiling of knee osteoarthritis patients identifies baseline characteristics associated with positive response to autologous platelet-rich plasma injection at one-year follow-up.Frontiers in immunology · 2026Article
- Integrated RNA-seq and scRNA-seq to explore the biological mechanisms of mitophagy-related genes in ulcerative colitis.PloS one · 2026Article
- Virus-inspired lipopeptide-derived nucleic acid delivery to cartilage for osteoarthritis therapy.Nature communications · 2025Article
- Atrial Fibroblasts-Derived Extracellular Vesicles Exacerbate Atrial Arrhythmogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CRP-Albumin-Lymphocyte index (CALLYI) as a risk-predicting biomarker in association with osteoarthritis.Arthritis research & therapy · 2025Article
- Disease-Associated Signatures Persist in Extracellular Vesicles from Reprogrammed Cells of Osteoarthritis Patients.International journal of molecular sciences · 2025Article
- Pyroptosis for osteoarthritis treatment: insights into cellular and molecular interactions inflammatory.Frontiers in immunology · 2025Review
- Acute phase proteins patterns as biomarkers in bacterial infection: Recent insights.Open veterinary journal · 2024Review
- Macrophage-derived ectosomal miR-350-3p promotes osteoarthritis progression through downregulating chondrocyte H3K36 methyltransferase NSD1.Cell death discovery · 2024Article
- Role of crosstalk between synovial cells and chondrocytes in osteoarthritis (Review).Experimental and therapeutic medicine · 2024Review
- Bioinformatics and Integrative Experimental Method to Identifying and Validating Co-Expressed Ferroptosis-Related Genes in OA Articular Cartilage and Synovium.Journal of inflammation research · 2024Article
- Case report: Cytokine and miRNA profiling in multisystem inflammatory syndrome in children.Frontiers in medicine · 2024Article
- Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes.Frontiers in medicine · 2024Review
- Article
- Arthritic Microenvironment-Dictated Fate Decisions for Stem Cells in Cartilage Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Urchin-like ceria nanoparticles for enhanced gene therapy of osteoarthritis.Science advances · 2023Article
- Macrophages in immunoregulation and therapeutics.Signal transduction and targeted therapy · 2023Review
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has shown an imbalance in M1/M2 macrophage polarization to play an essential role in osteoarthritis (OA) progression. However, the underlying mechanistic basis for this polarization is unknown. RNA sequencing of OA M1-polarized macrophages found highly expressed levels of pentraxin 3 (PTX3), suggesting a role for PTX3 in OA occurrence and development. Herein, PTX3 was found to be increased in the synovium and articular cartilage of OA patients and OA mice. Intra-articular injection of PTX3 aggravated, while PTX3 neutralization reversed synovitis and cartilage degeneration. No metabolic disorder or proteoglycan loss were observed in cartilage explants when treated with PTX3 alone. However, cartilage explants exhibited an OA phenotype when treated with culture supernatants of macrophages stimulated with PTX3, suggesting that PTX3 did not have a direct effect on chondrocytes. Therefore, the OA anti-chondrogenic effects of PTX3 are primarily mediated through macrophages. Mechanistically, PTX3 was upregulated by miR-224-5p deficiency, which activated the p65/NF-κB pathway to promote M1 macrophage polarization by targeting CD32. CD32 was expressed by macrophages, that when stimulated with PTX3, secreted abundant pro-inflammation cytokines that induced severe articular cartilage damage. The paracrine interaction between macrophages and chondrocytes produced a feedback loop that enhanced synovitis and cartilage damage. The findings of this study identified a functional pathway important to OA development. Blockade of this pathway and PTX3 may prevent and treat OA.
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