ArticleScientific reports2025
Bone marrow mesenchymal stem cell exosome-derived miR-223 regulated cellular pyroptosis of macrophage in osteomyelitis through regulating LACC1.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Context-dependent roles of the NLRP3 inflammasome in osteomyelitis and strategies for precision modulation.Frontiers in immunology · 2026Review
- Therapeutic Potential of Exosomes in Bone Infection: Mechanisms of Action, Engineering Strategies, and Translational Applications.International journal of nanomedicine · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Osteomyelitis (OM) is a severe bone infection characterized by inflammation and tissue damage. Macrophages play a crucial role in the inflammatory response during OM, and exosomes derived from bone marrow mesenchymal stem cells (BMSCs) have been proposed as potential therapeutic agents. Previous studies suggest that miR-223, a microRNA involved in inflammatory processes, is dysregulated in OM. This study investigates the role of BMSCs-derived exosomes carrying miR-223 in regulating macrophage pyroptosis, a form of programmed cell death triggered by inflammation. Blood samples were collected from OM patients and control subjects to assess miR-223 expression. BMSCs were treated with LPS to simulate the OM environment. Exosomes were extracted from miR-223 overexpressing BMSCs and characterized. The effects of these exosomes on macrophage survival, apoptosis, and pyroptosis were assessed through CCK-8 assays, flow cytometry, TUNEL staining, ELISA, and western blotting. The miR-223-mediated regulation of Caspase-1 and LACC1 expression was evaluated using specific inhibitors and gene expression analysis. miR-223 expression was significantly reduced in OM patients and in LPS-treated BMSCs. BMSCs-derived exosomes carrying miR-223 (miR-223 exo) enhanced macrophage viability, reduced apoptosis, and mitigated LPS-induced pyroptosis by targeting the NLRP3 inflammasome and Caspase-1 expression. Co-treatment with miR-223 inhibitors and Caspase-1 inhibitors showed that miR-223 regulated macrophage survival and inflammation through Caspase-1 modulation. Further investigation revealed that miR-223 targeted LACC1 to alleviate macrophage pyroptosis, with LACC1 overexpression reversing the protective effects of miR-223. BMSCs-derived exosomes carrying miR-223 play a protective role in OM by regulating macrophage pyroptosis and inflammation. This effect is mediated through the modulation of Caspase-1 and LACC1 expression, highlighting the potential of miR-223-based therapies for OM treatment.
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