ArticleRegenerative therapy2024
Epigenetic mechanism of miR-26b-5p-enriched MSCs-EVs attenuates spinal cord injury.
Article in Regenerative therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 7 citations in OpenAlex.
- Investigation of MicroRNA Expression Levels in Peripheral Blood of Turkish Males with Cocaine Use Disorder.Epigenomes · 2026Article
- Molecular Mechanism of M2 Macrophage-Derived Extracellular Vesicles in Alleviating Inflammation in Rats with Spinal Cord Injury.Neurochemical research · 2026Article
- Exercise training promotes nerve cell repair and regeneration after spinal cord injury.Neural regeneration research · 2026Article
- Current research progress on extracellular vesicles derived from mesenchymal stem cells in tuberculosis treatment (Review).Molecular medicine reports · 2026Review
- Targeting the glial-fibrotic scar microenvironment after spinal cord injury: From integrated protection to systematic regulation of regenerative balance.Journal of orthopaedic translation · 2026Review
- Schistosoma japonicum peptide SJMHE1 promotes peripheral nerve regeneration via macrophage migrasome-derived miR-26b-5p targeting the PTEN/AKT axis.Journal of translational medicine · 2025Article
- Extracellular Vesicles as Epigenetic Regulators of Redox Homeostasis: A Systematic Review and Meta-Analysis.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Extracellular vesicle therapy in neurological disorders.Journal of biomedical science · 2024Review
- Exosomes from preconditioned mesenchymal stem cells: Tissue repair and regeneration.Regenerative therapy · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesenchymal stem cells (MSCs) and extracellular vesicles (EVs) are promising therapies for the treatment of spinal cord injury (SCI). This study sought to explore the epigenetic mechanism of miR-26b-5p-enriched MSCs-EVs in SCI. MSCs and MSCs-EVs were isolated and characterized. The SCI rat model was established, followed by Basso-Beattie-Bresnahan scoring and H&E staining. In vitro cell models were established in PC12 cells with lipopolysaccharide (LPS) treatment, followed by cell viability evaluation using CCK-8 assay. The levels of miR-26b-5p, lysine demethylase 6A (KDM6A), NADPH oxidase 4 (NOX4), reactive oxygen species (ROS), and inflammatory factors (TNF-α/IL-1β/IL-6) in tissues and cells were detected. The levels of cy3-lablled miR-26b-5p in tissues and cells were observed by confocal microscopy. The binding of miR-26b-5p to KDM6A 3'UTR and the enrichments of KDM6A and H3K27me3 at the NOX4 promoter were analyzed. MSCs-EVs attenuated motor dysfunction, inflammation, and oxidative stress in SCI rats. MSCs-EVs delivered miR-26b-5p into PC12 cells to reduce LPS-induced inflammation and ROS production and enhance cell viability. miR-26b-5p inhibited KDM6A, and KDM6A reduced H3K27me3 at the NOX4 promoter to promote NOX4. Overexpression of KDM6A or NOX4 reversed the alleviative role of MSCs-EVs in SCI or LPS-induced cell injury. Overall, MSCs-EVs delivered miR-26b-5p into cells to target the KDM6A/NOX4 axis and facilitate the recovery from SCI.
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Registered trials
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