miR‐124 Contributes to the functional maturity of microglia
Abstract
During early development of the central nervous system (CNS), a subset of yolk‐sac derived myeloid cells populate the brain and provide the seed for the microglial cell population, which will self‐renew throughout life. As development progresses, individual microglial cells transition from a phagocytic amoeboid state through a transitional morphing phase into the sessile, ramified, and normally nonphagocytic microglia observed in the adult CNS under healthy conditions. The molecular drivers of this tissue‐specific maturation profile are not known. However, a survey of tissue resident macrophages identified miR‐124 to be expressed in microglia. In this study, we used transgenic zebrafish to overexpress miR‐124 in the mpeg1 expressing yolk‐sac‐derived myeloid cells that seed the microglia. In addition, a systemic sponge designed to neutralize the effects of miR‐124 was used to assess microglial development in a miR‐124 loss‐of‐function environment. Following the induction of miR‐124 overexpression, microglial motility and phagocytosis of apoptotic cells were significantly reduced. miR‐124 overexpression in microglia resulted in the accumulation of residual apoptotic cell bodies in the optic tectum, which could not be achieved by miR‐124 overexpression in differentiated neurons. Conversely, expression of the miR‐124 sponge caused an increase in the motility of microglia and transiently rescued motility and phagocytosis functions when activated simultaneously with miR‐124 overexpression. This study provides in vivo evidence that miR‐124 activity has a key role in the development of functionally mature microglia. © 2015 Wiley Periodicals, Inc. Develop Neurobiol 76: 507–518, 2016
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miR-124 is identified in microglia but not in other macrophages.
“MiR-124 was identified in microglia, but not in other macrophages.”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [234]
In zebrafish, overexpression of miR-124 reduces microglia motility and phagocytosis, causing accumulation of residual apoptotic cell bodies in the optic tectum.
“In a zebrafish model it was demonstrated that overexpression of miR-124 reduces microglia motility and phagocytosis, which resulted in accumulation of residual apoptotic cell bodies in the optic tectum [234].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [234]
miR-124 is a brain-enriched microRNA that is highly expressed in microglia and is critical for maintaining microglia in a quiescent state.
“MicroRNA-124 (miR-124), a brain-enriched microRNA, is known to regulate microglial quiescence.”
From Engineered Extracellular Vesicles Loaded With miR-124 Attenuate Cocaine-Mediated Activation of Microglia (2020) · cites this paper as Svahn et al., 2016
miR-124 is highly expressed in microglia and is critical for maintaining microglia in a quiescent state.
“It has been well-recognized that miR-124 is highly expressed in microglia and is critical for maintaining microglia in a quiescent state (Ponomarev et al., 2011; Veremeyko et al., 2013; Svahn et al., 2016).”
From Engineered Extracellular Vesicles Loaded With miR-124 Attenuate Cocaine-Mediated Activation of Microglia (2020) · cites this paper as Svahn et al., 2016
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- Authors
- Svahn, A. J., Giacomotto, J., Graeber, M. B., Rinkwitz, S., & Becker, T. S.
- Affiliations
- The University of Sydney (AU)
- Corresponding author
- Becker, Thomas S.
- Venue
- Developmental Neurobiology
- Publisher
- Wiley
- Published
- 2015-07-25
- Volume
- 76
- Issue
- 5
- Pages
- 507-518
- ISSN
- 1932-8451 (ISSN-L)
- 1932-846X
- OpenAlex
- W2146247875
- Cited by
- 42
- References
- 54
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 3 · 2022: 7 · 2021: 1 · 2020: 4 · 2019: 6 · 2018: 4 · 2017: 3 · 2016: 9
- FWCI
- 2.85
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Developmental Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Australian Research Council (ARC DP150104472)
- National Health and Medical Research Council (NHMRC APP1010713)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- miR-124, microglial development, microglial maturation, microglial motility, phagocytosis of apoptotic cells, microglial phagocytosis, zebrafish, microRNA sponge, optic tectum, central nervous system development
- MeSH terms
- Animals, Cell Movement, Cell Survival, Macrophages, Membrane Proteins, Neurons, Phagocytosis, Superior Colliculi, Zebrafish, Apoptosis, Sequence Homology, Microglia, Zebrafish Proteins, Animals, Genetically Modified, MicroRNAs, Gene Knockdown Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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