ArticleJournal of orthopaedic surgery and research2025
Insights into the potential role of BMSCs-exo delivered USP14 on SIRT1 deubiquitination in Staphylococcus aureus-induced model of osteomyelitis.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Osteomyelitis: Epidemiology, Classification, Pathophysiology, Clinical Features, Diagnosis, and Management.MedComm · 2026Review
- Therapeutic Potential of Exosomes in Bone Infection: Mechanisms of Action, Engineering Strategies, and Translational Applications.International journal of nanomedicine · 2026Review
- FTO-engineered extracellular vesicles from bone marrow mesenchymal stem cells ameliorate Staphylococcus aureus-induced osteomyelitis via m6A-dependent suppression of autophagy and pyroptosis.Journal of biological engineering · 2025Article
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5 authors.
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Abstract
Osteomyelitis resulting from a traumatic fracture is a recurrent and difficult-to-treat bone infection. Ubiquitin-specific protease 14 (USP14), a deubiquitinating enzyme, and Sirtuin-1 (SIRT1), an NAD+-dependent deacetylase, both play critical roles in regulating cellular processes, including inflammation. It has been discovered that exosomes originated from bone marrow mesenchymal stem cells (BMSCs-exo) can promote the repair and regeneration of bone fractures. In this study, we aimed to investigate the role of BMSCs-exo in osteoblast differentiation in osteomyelitis and the related molecular mechanisms. MC3T3-E1 cells induced with S. aureus were used as an in vitro model of osteomyelitis. BMSCs-exo were isolated and characterized using ultracentrifugation, transmission electron microscopy (TEM), and Western blot. RT-qPCR, Western blot, CCK-8, ALP staining, ELISA, and CO-IP were utilized to evaluate USP14 and SIRT1 levels, the osteogenic differentiation ability of MC3T3-E1 cells, and the deubiquitination level of SIRT1. Low expression of USP14 and SIRT1 was observed in the bone tissue of osteomyelitis patients. BMSCs-exo could upregulate the expression of USP14 and promote the expression of SIRT1 protein in the cell model of osteomyelitis. In addition, BMSCs-exo reduced the levels of inflammatory factors TNFα and IL-6, enhanced cell viability, promoted the expression of osteogenic differentiation markers RUNX2 and OCN in MC3T3-E1 cells, and improved cell osteogenic capacity. However, these trends were significantly reversed in MC3T3-E1 cells following treatment with BMSCs-exo transfected with si-USP14. Furthermore, knockdown of USP14 promoted SIRT1 ubiquitination and degradation, the process that was reversed by the proteasome inhibitor MG132, whereas USP14 overexpression inhibited SIRT1 ubiquitination. In MC3T3-E1 cells infected with S. aureus, BMSCs-exo delivers USP14, which may enhance SIRT1 deubiquitination and increase SIRT1 protein activity. This process inhibits inflammation and promotes osteogenesis, warranting further investigation into its mechanisms and in vivo efficacy.
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