ArticleJournal of translational medicine2024
Transplantation of miR-145a-5p modified M2 type microglia promotes the tissue repair of spinal cord injury in mice.
Article in Journal of translational medicine, 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.
- M2 microglia-derived migrasome-enriched extracellular vesicles restore mitochondrial homeostasis to orchestrate neurovascular unit recovery after ischemic stroke.Journal of nanobiotechnology · 2026Article
- Construction of a Computationally Inferred Single-Cell miRNA Activity Atlas and Analysis of Regulatory Networks in Spinal Cord Injury.Journal of molecular neuroscience : MN · 2026Article
- Beyond Transplantation: Engineering Neural Cell Therapies and Combination Strategies for Spinal Cord Repair.Brain sciences · 2026Review
- METTL3 regulates Leydig cell proliferation via miR-145-PCK1 mediated gluconeogenesis in goats.Journal of animal science and biotechnology · 2026Article
- The role of immune regulation in peripheral nerve regeneration: functions of inflammatory cells and cytokines.Frontiers in pharmacology · 2026Review
- The clinical significance of miR-18a-3p in traumatic spinal cord injury and its functional role in mediating apoptosis, inflammation and oxidative stress.Journal of orthopaedic surgery and research · 2025Article
- ELAVL1-mediated USP29 mRNA degradation activates TAK1 driving M1 microglial polarization and neural stem cell differentiation dysregulation in spinal cord injury.Cell death discovery · 2025Article
- Comprehensive review of macrophage models: primary cells and immortalized lines across species.Frontiers in immunology · 2025Review
- Neuroinflammation: targeting microglia for neuroprotection and repair after spinal cord injury.Frontiers in immunology · 2025Review
- Evolving insights on the role of microglia in neuroinflammation, plasticity, and regeneration of the injured spinal cord.Frontiers in immunology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundThe traumatic spinal cord injury (SCI) can cause immediate multi-faceted function loss or paralysis. Microglia, as one of tissue resident macrophages, has been reported to play a critical role in regulating inflammation response during SCI processes. And transplantation with M2 microglia into SCI mice promotes recovery of motor function. However, the M2 microglia can be easily re-educated and changed their phenotype due to the stimuli of tissue microenvironment. This study aimed to find a way to maintain the function of M2 microglia, which could exert an anti-inflammatory and pro-repair role, and further promote the repair of spinal cord injury.
methodsTo establish a standard murine spinal cord clip compression model using Dumont tying forceps. Using FACS, to sort microglia from C57BL/6 mice or CX3CR1
resultsWith in vitro experiments, we found that miR-145a-5p was highly expressed in M2 microglia, and miR-145a-5p overexpression could suppress M1 while promote M2 microglia polarization. And then delivery of miR-145a-5p overexpressed M2 microglia into the injured spinal cord area significantly accelerated locomotive recovery as well as prevented glia scar formation and neuron damage in mice, which was even better than M2 microglia transplantation. Further mechanisms showed that overexpressed miR-145a-5p in microglia inhibited the inflammatory response and maintained M2 macrophage phenotype by targeting TLR4/NF-κB signaling.
conclusionsThese findings indicate that transplantation of miR-145a-5p modified M2 microglia has more therapeutic potential for SCI than M2 microglia transplantation from epigenetic perspective.
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