ArticleCell death & disease2019
Inhibition of microRNA-711 limits angiopoietin-1 and Akt changes, tissue damage, and motor dysfunction after contusive spinal cord injury in mice.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Platelet-rich plasma-primed bone marrow mesenchymal stem cell-derived exosomes inhibit neuronal apoptosis and autophagy, and promote nerve regeneration via the miR-29a-3p/PTEN/PI3K/Akt/mTOR axis after spinal cord injury.Journal of molecular histology · 2026Article
- Circulating microRNA Profiles in Acute Spinal Cord Injury: Evidence for Distinct Plasma Signatures Compared with Polytrauma Patients.International journal of molecular sciences · 2025Article
- Identification of a New Role of miR-199a-5p as Factor Implied in Neuronal Damage: Decreasing the Expression of Its Target X-Linked Anti-Apoptotic Protein (XIAP) After SCI.International journal of molecular sciences · 2024Article
- Spinal cord injury disrupts plasma extracellular vesicles cargoes leading to neuroinflammation in the brain and neurological dysfunction in aged male mice.Brain, behavior, and immunity · 2024Article
- Circ_0006640 transferred by bone marrow-mesenchymal stem cell-exosomes suppresses lipopolysaccharide-induced apoptotic, inflammatory and oxidative injury in spinal cord injury.Journal of orthopaedic surgery and research · 2024Article
- Brain injury accelerates the onset of a reversible age-related microglial phenotype associated with inflammatory neurodegeneration.Science advances · 2023Article
- MicroRNA-299a-5p Protects against Spinal Cord Injury through Activating AMPK Pathway.Oxidative medicine and cellular longevity · 2022Article
- Identification of key pathways and RNAs associated with skeletal muscle atrophy after spinal cord injury.Journal of musculoskeletal & neuronal interactions · 2021Article
- Therapeutic targets and nanomaterial-based therapies for mitigation of secondary injury after spinal cord injury.Nanomedicine (London, England) · 2021Review
- MiR-122-5p Mitigates Inflammation, Reactive Oxygen Species and SH-SY5Y Apoptosis by Targeting CPEB1 After Spinal Cord Injury Via the PI3K/AKT Signaling Pathway.Neurochemical research · 2021Article
- Article
- Mechanism of mesenchymal stem cells in spinal cord injury repair through macrophage polarization.Cell & bioscience · 2021Review
- The voltage-gated proton channel Hv1 plays a detrimental role in contusion spinal cord injury via extracellular acidosis-mediated neuroinflammation.Brain, behavior, and immunity · 2021Article
- Reactive Astrocytes in Central Nervous System Injury: Subgroup and Potential Therapy.Frontiers in cellular neuroscience · 2021Review
- MiR-211 protects cerebral ischemia/reperfusion injury by inhibiting cell apoptosis.Bioengineered · 2020Article
- Identification of Circular RNA Expression Profiles and their Implication in Spinal Cord Injury Rats at the Immediate Phase.Journal of molecular neuroscience : MN · 2020Article
- Catalpol Protects Against Spinal Cord Injury in Mice Through Regulating MicroRNA-142-Mediated HMGB1/TLR4/NF-κB Signaling Pathway.Frontiers in pharmacology · 2020Article
- GPNMB Modulates Autophagy to Enhance Functional Recovery After Spinal Cord Injury in Rats.Cell transplantationArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Spinal cord injury (SCI) causes neuronal cell death and vascular damage, which contribute to neurological dysfunction. Given that many biochemical changes contribute to such secondary injury, treatment approaches have increasingly focused on combined therapies or use of multi-functional drugs. MicroRNAs (miRs) are small (20-23 nucleotide), non-protein-coding RNAs and can negatively regulate target gene expression at the post-transcriptional level. As individual miRs can potentially modulate expression of multiple relevant proteins after injury, they are attractive candidates as upstream regulators of the secondary SCI progression. In the present study we examined the role of miR-711 modulation after SCI. Levels of miR-711 were increased in injured spinal cord early after SCI, accompanied by rapid downregulation of its target angiopoietin-1 (Ang-1), an endothelial growth factor. Changes of miR-711 were also associated with downregulation of the pro-survival protein Akt (protein kinase B), another target of miR-711, with sequential activation of glycogen synthase kinase 3 and the pro-apoptotic BH3-only molecule PUMA. Central administration of a miR-711 hairpin inhibitor after SCI limited decreases of Ang-1/Akt expression and attenuated apoptotic pathways. Such treatment also reduced neuronal/axonal damage, protected microvasculature and improved motor dysfunction following SCI. In vitro, miR-711 levels were rapidly elevated by neuronal insults, but not by activated microglia and astrocytes. Together, our data suggest that post-traumatic miR-711 elevation contributes to neuronal cell death after SCI, in part by inhibiting Ang-1 and Akt pathways, and may serve as a novel therapeutic target.
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