ArticleJournal of orthopaedic surgery and research2025
USP15-modified ADMSCs-Exo alleviates chondrocyte damage and effectively relieved osteoarthritis by inducing M2 polarization of macrophages through deubiquitinating FOXC1.
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 6 papers.
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Who cites it
6 citing papers in PubMed.
- Small extracellular vesicles in osteoarthritis: A double‑edged sword regulating inflammation and cartilage homeostasis (Review).International journal of molecular medicine · 2026Review
- Mesenchymal stromal cells therapy for remodeling the joint microenvironment: mechanisms, nanotechnology-enhanced strategies, and translation prospects.Stem cell research & therapy · 2026Review
- The role of stem cells and their engineering strategies in the repair of nerve damage in intracerebral hemorrhage.Cell & bioscience · 2026Review
- USP15-dependent modulation of TGF-β/Smad2/3 signaling: implications for chondrocyte matrix degradation and autophagy in osteoarthritis.Scientific reports · 2025Article
- Y-box binding protein 1 stabilizes EP300 mRNA and promotes forkhead box C1 H3K27Ac to aggravate chondrocyte injury in osteoarthritis.Journal of cell communication and signaling · 2025Article
- Phenotypic Changes and Oxidative Stress in THP-1 Macrophages in Response to Vanilloids Following Stimulation with Allergen Act d 1 and LPS.Antioxidants (Basel, Switzerland) · 2025Article
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Authors and funding
5 authors.
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Abstract
backgroundThe damage to chondrocytes and inflammatory responses are considered the key factors in the pathogenesis of osteoarthritis (OA). Ubiquitin-specific protease 15 (USP15) has been shown to be involved in OA. This study aimed to explore the mechanism of USP15-modified adipose-derived mesenchymal stem cells (ADMSCs) exosome (Exo) in alleviating OA.
methodsADMSC-Exo with USP15 overexpression was isolated by magnetic beads method, and the Exo marker proteins were identified by western blot assay. M1 and M2 phenotypic markers of THP1-M0 cells were analyzed by flow cytometry. ELISA was used to detect the expression of inflammatory factors in cells. CCK-8, EdU, Transwell, and flow cytometry were used to detect the cell activity, proliferation, apoptosis and migration ability. The interaction between forkhead box C1 (FOXC1) and USP15 was verified by Glutathione-S-transferase (GST) pull-down and Co-immunoprecipitation (Co-IP) experiments. The stability of FOXC1 was measured by cycloheximide (CHX), and its ubiquitination level was analyzed by exogenous ubiquitination assay.
resultsThe Exos from ADMSCs overexpressing USP15 (oe-USP15/Exos) were successfully isolated. It was confirmed that oe-USP15/Exo inhibited the M1 polarization of THP1-M0 cells caused by lipopolysaccharide (LPS) but induced the M2 polarization and the release of inflammatory inhibitory factors. Meanwhile, the damage of chondrocytes caused by LPS was also prevented by oe-USP15/Exo. Besides, USP15 was validated to exert a deubiquitination effect by binding to FOXC1 and positively regulate FOXC1 expression. And the effects of oe-USP15/Exo were abolished after FOXC1 silencing.
conclusionUSP15-modified ADMSC-derived Exos facilitated M2 polarization of macrophages and improved chondrocyte injury by deubiquitination of FOXC1.
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