ArticleACS applied materials & interfaces2025
Exosomes Derived from Tanshinone IIA-Pretreated Umbilical Cord Mesenchymal Stem Cells Repair Traumatic Spinal Cord Injury by miR-223-5p/USP8/NLRP3 Axis.
Article in ACS applied materials & interfaces, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Mesenchymal stem cells and secretome as modulators of neuroinflammation in neurological disorders.Journal of translational medicine · 2026Review
- Synergistic effects of tanshinone IIA and mesenchymal stem cells on neuroprotection, cardiovascular repair, tissue regeneration, muscle protein synthesis, and gut microbiota modulation across neurodegenerative, cardiovascular, and regenerative disease models.Frontiers in cell and developmental biology · 2026Review
- Exosomes as regenerative therapeutics for spinal cord injury: mechanisms and clinical prospects.Frontiers in medicine · 2026Review
- Upregulation of miR-502-5p in traumatic spinal cord injury modulates neuroinflammation and oxidative stress by targeting FBXO28.Journal of orthopaedic surgery and research · 2025Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) lacks effective therapies, and umbilical cord mesenchymal stem cell (UCMSC)-derived exosomes show promise but require efficacy optimization. This study explored tanshinone IIA (TSA)-pretreated UCMSC exosomes (T-Exos) to enhance neuroprotection and functional recovery post-SCI. T-Exos were isolated from the TSA-treated UCMSCs. SCI mice received T-Exos, with motor function assessed behaviorally. In vitro and in vivo, microglial NLRP3 inflammasome activity, polarization (M1/M2), and cytokine release were analyzed. miRNA profiling identified key miRNAs in T-Exos; miR-223-5p's role was validated via inhibition. Mechanistic studies linked miR-223-5p to USP8/NLRP3 using Western blot, qPCR, and co-IP assays. T-Exos improved motor recovery in SCI mice by suppressing NLRP3 inflammasome activation, shifting microglia to anti-inflammatory M2 phenotypes, reducing the level of IL-1β/IL-18, and alleviating oxidative stress. miR-223-5p was highly enriched in T-Exos, and its inhibition reversed therapeutic effects. Mechanistically, miR-223-5p targeted USP8, a deubiquitinase stabilizing NLRP3. By inhibiting USP8, T-Exos reduced NLRP3 levels, dampening neuroinflammation. TSA pretreatment enhances exosomal miR-223-5p, which blocks USP8-mediated NLRP3 stabilization, driving microglial M2 polarization and neuroprotection. These findings highlight T-Exos as a targeted therapy for SCI, offering insights into the exosome-mediated modulation of inflammatory microenvironments for neural repair.
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