ArticleJournal of neuroscience research2019
Neuronal extracellular microRNAs miR-124 and miR-9 mediate cell-cell communication between neurons and microglia.
Article in Journal of neuroscience research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Exosomes in depression: mechanistic insights, diagnostic potential, and therapeutic opportunities.Molecular psychiatry · 2026Review
- Targeting the microbiota-miRNA-protease axis: A new therapeutic avenue in melanoma.The FEBS journal · 2026Review
- Effects of Wheat Malt Extract on Molecular and Behavioral Markers in Aged APP/PS1 and Wild-Type Mice.International journal of molecular sciences · 2026Article
- APOE Lipoprotein Particles: Pathophysiology, Therapy, and the Crosstalk in Alzheimer's Disease and Cardiovascular Disease.Molecular neurobiology · 2025Review
- Extracellular vesicle-derived MicroRNAs as potential therapies for spinal cord and peripheral nerve injuries.RNA biology · 2025Review
- The Molecular Dynamics of Extracellular Vesicles and their Protein Corona in the Secretomes of Stem Cells.Stem cell reviews and reports · 2025Review
- MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis.Cellular and molecular neurobiology · 2025Review
- Neurodegenerative disease-associated microRNAs acting as signaling molecules modulate CNS neuron structure and viability.Cell communication and signaling : CCS · 2025Article
- Exosomes enriched with miR-124-3p show therapeutic potential in a new microfluidic triculture model that recapitulates neuron-glia crosstalk in Alzheimer's disease.Frontiers in pharmacology · 2025Article
- Extracellular Vesicles in the Central Nervous System: A Novel Mechanism of Neuronal Cell Communication.International journal of molecular sciences · 2024Review
- Article
- Hydrogen-rich saline alleviates cardiomyocyte apoptosis by reducing expression of calpain1 via miR-124-3p.ESC heart failure · 2023Article
- Modulation of the Cellular microRNA Landscape: Contribution to the Protective Effects of High-Density Lipoproteins (HDL).Biology · 2023Review
- Complement C4-deficient mice have a high mortality rate during PTZ-induced epileptic seizures, which correlates with cognitive problems and the deficiency in the expression of Egr1 and other immediate early genes.Frontiers in cellular neuroscience · 2023Article
- Inter-neuronal signaling mediated by small extracellular vesicles: wireless communication?Frontiers in molecular neuroscience · 2023Review
- Neuronal and Glial Communication via Non-Coding RNAs: Messages in Extracellular Vesicles.International journal of molecular sciences · 2022Review
- Engineering extracellular vesicles for Alzheimer's disease: An emerging cell-free approach for earlier diagnosis and treatment.WIREs mechanisms of disease · 2022Review
- Protective Signature of IFNγ-Stimulated Microglia Relies on miR-124-3p Regulation From the Secretome Released by Mutant APP Swedish Neuronal Cells.Frontiers in pharmacology · 2022Article
- MiRNA-124a: a Potential Biomarker for Neurological Deficits Following Cardiac Surgery in Pediatric Patients.Journal of cardiovascular translational research · 2021Article
- The promise of microRNA-based therapies in Alzheimer's disease: challenges and perspectives.Molecular neurodegeneration · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In contrast to peripheral macrophages, microglia in the central nervous system (CNS) exhibit a specific deactivated phenotype; however, it is not clear how this phenotype is maintained. Two alternative hypotheses were postulated recently: (a) microglia differ from peripheral macrophages being derived from the yolk sac (YS), whereas peripheral macrophages originate from bone marrow (BM); (b) microglia acquire a specific phenotype under the influence of the CNS microenvironment. We have previously shown that microglia express miR-124, which was also induced in BM-derived macrophages co-cultured with a neurons. We here investigated the possibility of horizontal transfer of the neuron-specific microRNAs miR-124 and miR-9 from primary neurons to microglia/macrophages. We found that after incubation with neuronal conditioned media (NCM), macrophages downregulated activation markers MHC class II and CD45. Neither cultured adult microglia nor YS- and BM-derived macrophages demonstrated intrinsic levels of miR-124 expression. However, after incubation with NCM, miR-124 was induced in both YS- and BM-derived macrophages. Biochemical analysis demonstrated that the NCM contained miR-124 and miR-9 in complex with small proteins, large high-density lipoproteins (HDLs), and exosomes. MiR-124 and miR-9 were promptly released from neurons, and this process was inhibited by tetrodotoxin, indicating an important role of neuronal electric activity in secretion of these microRNAs. Incubation of macrophages with exogenous miR-124 resulted in efficient translocation of miR-124 into the cytoplasm. This study demonstrates an important role of neuronal miRNAs in communication of neurons with microglia, which favors the hypothesis that microglia acquire a specific phenotype under the influence of the CNS microenvironment.
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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.