ArticleCell death & disease2019
Astrocytic miR-324-5p is essential for synaptic formation by suppressing the secretion of CCL5 from astrocytes.
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 29 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
29 citing papers in PubMed, 46 citations in OpenAlex.
- MiRNA Dysregulation in Epilepsy: Bridging Molecular Mechanisms and Therapeutic Innovation.Molecular neurobiology · 2026Review
- Pathological Roles of Astrocytes in Traumatic Brain Injury.CNS neuroscience & therapeutics · 2026Review
- CNTNAP2: isoform- and context-specific functions in neurological disorders and cancer.Frontiers in cellular neuroscience · 2026Review
- Impaired macroautophagy in oligodendrocyte precursor cells suppresses neuronal plasticity via a senescence-associated signaling.Science advances · 2025Article
- Overexpression of the Dicer family genes influences lifespan and stress resistance in a tissue-, sex-, and stressor-specific manner in Drosophila melanogaster.Biogerontology · 2025Article
- SAM Alleviates Neuroinflammation by Regulating M1/M2 Polarization of Microglia Through α7nAChR/Nrf2/HO-1 Signaling Pathway.Neurochemical research · 2025Article
- IL-1ra and CCL5, but not IL-10, are promising targets for treating SMA astrocyte-driven pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Neuronal injury and hepatotoxicity: astrocytes and stellate cells convergence and their role in tissue repair.Frontiers in neuroscience · 2025Review
- FABP7 drives an inflammatory response in human astrocytes and is upregulated in Alzheimer's disease.GeroScience · 2024Article
- Identification of novel microRNAs in the embryonic mouse brain using deep sequencing.Molecular and cellular biochemistry · 2024Article
- Spotlight on pro-inflammatory chemokines: regulators of cellular communication in cognitive impairment.Frontiers in immunology · 2024Review
- Mir324 knockout regulates the structure of dendritic spines and impairs hippocampal long-term potentiation.Scientific reports · 2023Article
- Age-Dependent Regulation of Dendritic Spine Density and Protein Expression in Mir324 KO Mice.Journal of molecular neuroscience : MN · 2023Article
- Age-dependent regulation of dendritic spine density and protein expression in Mir324 KO mice.Research square · 2023Article
- MicroRNA: A Linking between Astrocyte Dysfunction, Mild Cognitive Impairment, and Neurodegenerative Diseases.Life (Basel, Switzerland) · 2022Review
- A review on the role of miRNA-324 in various diseases.Frontiers in genetics · 2022Review
- Plasma microRNA vary in association with the progression of Alzheimer's disease.Alzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
- Cytokine Signalling at the Microglial Penta-Partite Synapse.International journal of molecular sciences · 2021Review
- Article
- Role of miRNA-324-5p-Modified Adipose-Derived Stem Cells in Post-Myocardial Infarction Repair.International journal of stem cells · 2021Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
There is accumulating evidence that astrocytes play an important role in synaptic formation, plasticity, and pruning. Dicer and the fine-tuning of microRNA (miRNA) network are important for maintaining the normal functions of central nervous system and dysregulation of miRNAs is implicated in neurological disorders. However, little is known about the role of Dicer and miRNAs of astrocytes in the homeostasis of synapse as well as its plasticity. By selectively deleting Dicer in postnatal astrocytes, Dicer-deficient mice exhibited reactive astrogliosis and deficits in dendritic spine formation. Astrocyte-conditioned medium (ACM) collected from Dicer-null astrocytes caused synapse degeneration in cultured primary neurons. The expression of chemokine ligand 5 (CCL5) elevated in Dicer-deleted astrocytes which led to the significant augmentation of secreted CCL5 in ACM. In neurons treated with Dicer KO-ACM, CCL5 supplementation inhibited MAPK/CREB signaling pathway and exacerbated the synaptic formation deficiency, while CCL5 knockdown partially rescued the synapse degeneration. Moreover, we validated CCL5 as miR-324-5p targeted gene. ACM collected from miR-324-5p antagomir-transfected astrocytes mimicked the effect of CCL5 treatment on inhibiting synapse formation and MAPK/CREB signaling in Dicer KO-ACM-cocultured neurons. Furthermore, decreased miR-324-5p expression and elevated CCL5 expression were observed in the brain of aging mice. Our work reveals the non-cell-autonomous roles of astroglial miRNAs in regulation of astrocytic secretory milieu and neuronal synaptogenesis, implicating the loss or misregulation of astroglial miRNA network may contribute to neuroinflammation, neurodegeneration, and aging.
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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.