ArticleExperimental biology and medicine (Maywood, N.J.)2021
miR-31 promotes neural stem cell proliferation and restores motor function after spinal cord injury.
Article in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Notch Signaling in Spinal Cord Injury: Mechanistic Insights and Therapeutic Perspectives.Molecular neurobiology · 2026Review
- Continuous intravenous infusion of human mesenchymal stromal cell-derived small extracellular vesicles in spinal cord injured rat modulates extracellular matrix and has greater therapeutic efficacy than multiple single injections.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Genome-Wide Identification of Microglia-Related RNA-Binding Proteins and Regulated Alternative Splicing in Spinal Cord Injury.ACS omega · 2025Article
- X inactive-specific transcript regulates mitochondrial function and neuronal differentiation of stem cellsWorld journal of stem cells · 2025Article
- Regulation of MicroRNAs After Spinal Cord Injury in Adult Zebrafish.Journal of molecular neuroscience : MN · 2024Article
- Recent advances in endogenous neural stem/progenitor cell manipulation for spinal cord injury repair.Theranostics · 2023Review
- Thyclotides, tetrahydrofuran-modified peptide nucleic acids that efficiently penetrate cells and inhibit microRNA-21.Nucleic acids research · 2022Article
- MiR-31 improves spinal cord injury in mice by promoting the migration of bone marrow mesenchymal stem cells.PloS one · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aims to examine whether miR-31 promotes endogenous NSC proliferation and be used for spinal cord injury management. In the present study, the morpholino knockdown of miR-31 induced abnormal neuronal apoptosis in zebrafish, resulting in impaired development of the tail. miR-31 agomir transfection in NSCs increased Nestin expression and decreased ChAT and GFAP expression levels. miR-31 induced the proliferation of mouse NSCs by upregulating the Notch signaling pathway, and more NSCs entered G1; Notch was inhibited by miR-31 inactivation. Injection of a miR-31 agomir into mouse models of spinal cord injury could effectively restore motor functions after spinal cord injury, which was achieved by promoting the proliferation of endogenous NSCs. After the injection of a miR-31 agomir in spinal cord injury mice, the expression of Nestin and GFAP increased, while GFAP expression decreased. In conclusion, the zebrafish experiments prove that a lack of miR-31 will block nervous system development. In spinal cord injury mouse models, miR-31 overexpression might promote spinal cord injury repair.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.