ArticleNeurochemical research2019
Increases in miR-124-3p in Microglial Exosomes Confer Neuroprotective Effects by Targeting FIP200-Mediated Neuronal Autophagy Following Traumatic Brain Injury.
Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.
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Who cites it
81 citing papers in PubMed, 2 syntheses or guidelines pooled it, 119 citations in OpenAlex.
- Efficacy of extracellular vesicles of different cell origins in traumatic brain injury: A systematic review and network meta-analysis.Frontiers in neuroscience · 2023Pooled it
- New Insight of Circular RNAs' Roles in Central Nervous System Post-Traumatic Injury.Frontiers in neuroscience · 2021Pooled it
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- The Dual Roles of Extracellular Vesicle Subtypes in Regulating Traumatic Brain Injury.International journal of molecular sciences · 2026Review
- Impact of Microglia-Derived Extracellular Vesicles on Resident Central Nervous System Cell Populations After Acute Brain Injury Under Various External Stimuli Conditions.Molecular neurobiology · 2025Review
- Neural Stem Cell-Derived Extracellular Vesicles for Advanced Neural Repair.Journal of neurochemistry · 2025Review
- Advances in research on biomaterials and stem cell/exosome-based strategies in the treatment of traumatic brain injury.Acta pharmaceutica Sinica. B · 2025Review
- The Application of MicroRNAs in Traumatic Brain Injury: Mechanism Elucidation and Clinical Translation.Molecular neurobiology · 2025Review
- Precision exosome engineering for neurological therapeutics: molecular mechanisms and targeted strategies.Molecular biology reports · 2025Review
- Extracellular vesicles in age-related diseases: disease pathogenesis, intervention, and biomarker.Stem cell research & therapy · 2025Review
- Genetic deletion of G protein-coupled receptor 56 aggravates traumatic brain injury through the microglial CCL3/4/5 upregulation targeted to CCR5.Cell death & disease · 2025Article
- The Role of Small Extracellular Vesicles Derived from Glial Cells in the Central Nervous System under both Normal and Pathological Conditions.Neurochemical research · 2025Review
- Exosomal MiRNA Therapy for Central Nervous System Injury Diseases.Cellular and molecular neurobiology · 2024Review
- Bioactive hydrogel synergizes neuroprotection, macrophage polarization, and angiogenesis to improve repair of traumatic brain injury.Materials today. Bio · 2024Article
- The role of autophagy in brain health and disease: Insights into exosome and autophagy interactions.Heliyon · 2024Review
- The Yin and Yang of Microglia-Derived Extracellular Vesicles in CNS Injury and Diseases.Cells · 2024Review
- Target specification and therapeutic potential of extracellular vesicles for regulating corneal angiogenesis, lymphangiogenesis, and nerve repair.The ocular surface · 2024Review
- Exosomes: A Cellular Communication Medium That Has Multiple Effects On Brain Diseases.Molecular neurobiology · 2024Review
- Extracellular vesicle therapy in neurological disorders.Journal of biomedical science · 2024Review
- Applications of Stem Cell-Derived Extracellular Vesicles in Nerve Regeneration.International journal of molecular sciences · 2024Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our recent study, we observed consistent increases in miR-124-3p levels in exosomes derived from cultured BV2 microglia which was treated with repetitive traumatic brain injury (rTBI) mouse model brain extracts. To clarify the mechanisms underlying increases in microglia-derived exosomal miR-124-3p and their role in regulating neuronal autophagy after TBI, we investigated the impact of exosomal miR-124-3p on neuronal autophagy in scratch-injured HT22 neurons and rTBI mice. We harvested injured brain extracts from rTBI mice at 3 to 21 days post injury (DPI) for the treatment of cultured BV2 microglia in vitro. We observed significant induction of autophagy following TBI in vitro, and that inhibition of activated neuronal autophagy could protect against trauma-induced injury. Our results indicated that co-culture of injured HT22 neurons with miR-124-3p overexpressing BV2 microglia exerted a protective effect by inhibiting neuronal autophagy in scratch-injured neurons. Further research revealed that these effects were achieved mainly via upregulation of exosomal miR-124-3p, and that Focal adhesion kinase family-interacting protein of 200 kDa (FIP200) plays a key role in trauma-induced autophagy. Injection of exosomes into the vena caudalis in in vivo experiments revealed that exosomal miR-124-3p was associated with decreases in the modified neurological severity score (mNSS) and improvements in Morris water maze (MWM) test results in rTBI mice. Altogether, our results indicate that increased miR-124-3p in microglial exosomes following TBI may inhibit neuronal autophagy and protect against nerve injury via their transfer into neurons. Thus, treatment with microglial exosomes enriched with miR-124-3p may represent a novel therapeutic strategy for the treatment of nerve injury after TBI.
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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.