Neuronal extracellular vesicle derived miR-98 prevents salvageable neurons from microglial phagocytosis in acute ischemic stroke
Open accessAbstract
Extracellular vesicles (EVs), as a novel intercellular communication carrier transferring cargo microRNAs (miRNAs), could play important roles in the brain remodeling process after ischemic stroke. However, the detailed mechanisms involved in EVs derived miRNAs-mediated cellular interactions in the brain remain unclear. Several studies indicated that microRNA-98 (miR-98) might participate in the pathogenesis of ischemic stroke. Here, we showed that expression of miR-98 in penumbra field kept up on the first day but dropped sharply on the 3rd day after ischemic stroke in rats, indicating that miR-98 could function as an endogenous protective factor post-ischemia. Overexpression of miR-98 targeted inhibiting platelet activating factor receptor-mediated microglial phagocytosis to attenuate neuronal death. Furthermore, we showed that neurons transferred miR-98 to microglia via EVs secretion after ischemic stroke, to prevent the stress-but-viable neurons from microglial phagocytosis. Therefore, we reveal that EVs derived miR-98 act as an intercellular signal mediating neurons and microglia communication during the brain remodeling after ischemic stroke. The present work provides a novel insight into the roles of EVs in the stroke pathogenesis and a new EVs-miRNAs-based therapeutic strategy for stroke.
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In murine ischemic stroke, surviving neurons synthesize miR-98, loaded into extracellular vesicles and transferred to microglia, preventing stressed but-viable neurons from microglial phagocytosis at least partially by targeting platelet activating factor receptor.
“In a murine model of ischemic stroke, it was demonstrated that surviving neurons synthesize miR-98, which is loaded into extracellular vesicles and transferred to microglia. Overall, this prevents stressed but-viable neurons from microglial phagocytosis, at least partially by targeting platelet activating factor receptor in microglia [231].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [231]
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- Authors
- Yang, J., Cao, L.-L., Wang, X.-P., Guo, W., Guo, R.-B., Sun, Y.-Q., Xue, T.-F., Cai, Z.-Y., Ji, J., Cheng, H., & Sun, X.-L.
- Affiliations
- Nanjing Medical University (CN)
- Jiangsu Province Hospital (CN)
- Nanjing University of Chinese Medicine (CN)
- Corresponding author
- Sun, Xiu-Lan
- Venue
- Cell Death & Disease
- Published
- 2021-01-06
- Volume
- 12
- Issue
- 1
- Pages
- 23-23
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC7791117
- OpenAlex
- W3119238477
- Cited by
- 73
- References
- 60
- Citations by year
- 2026: 6 · 2025: 17 · 2024: 7 · 2023: 12 · 2022: 18 · 2021: 13
- FWCI
- 3.92
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Jiangsu Commission of Health (ZDA2020006)
- National Natural Science Foundation of China (81973301, 81773701)
- Government of Jiangsu Province
- Nanjing Medical University (NMUD2018008)
- Jiangsu Provincial Key Research and Development Program (BE2017737)
- Natural Science Research of Jiangsu Higher Education Institutions of China (18KJA310004)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- extracellular vesicles, miR-98, microglial phagocytosis, acute ischemic stroke, neuronal cell death, platelet-activating factor receptor, neuron-microglia communication, penumbra, neuroprotection, stroke treatment
- MeSH terms
- Extracellular Vesicles, Ischemic Stroke, Acute Disease, Animals, Brain Ischemia, Disease Models, Animal, Humans, Neurons, Phagocytosis, Microglia, MicroRNAs, Rats
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