ArticleJournal of inflammation research2024
M1 Microglia-Derived Exosomes Promote A1 Astrocyte Activation and Aggravate Ischemic Injury via circSTRN3/miR-331-5p/MAVS/NF-κB Pathway.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Penumbra-derived small extracellular vesicles carry pathogenic RNA driving remote damage after cortical infarction.Brain : a journal of neurology · 2026Article
- The Dual Roles of Microglia- and Astrocyte-Derived Exosomes in Cerebral Ischemia-Reperfusion Injury: from Intercellular Communication to Therapeutic Prospects.Molecular neurobiology · 2026Review
- Dysregulation of exosomal miRNAs in A2 astrocytes under oxygen-glucose deprivation is associated with neuronal pyroptosis: a role for miR-139-5p in targeting NLRP3.Journal of orthopaedic surgery and research · 2026Article
- Prelimbic cortex to zona incerta pathway mediates recognition memory recovery delay through down-regulating astrocytic GAT-3.iScience · 2026Article
- Neurovascular Unit-Derived Extracellular Vesicles as Regulators of Post-Stroke Pathology and Neurorestoration.Biomolecules · 2026Review
- Acupuncture's Regulatory Role in Glial Cells and Their Interactions for Antidepressant Effects: A Review of Research Progress.Journal of multidisciplinary healthcare · 2026Review
- Glial-Dopamine crosstalk: Astrocytic and microglial gatekeepers of neuroinflammation, plasticity, and motivation.AIMS neuroscience · 2026Review
- Microglia-Derived Exosomal miR-223-3p Targets the RhoB-NF-κB-CCL11 Axis in Astrocytes and Relieves Neuronal Damage in Subarachnoid Hemorrhage.Neurochemical research · 2025Article
- Microglia-astrocyte crosstalk following ischemic stroke.Molecular brain · 2025Review
- Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: After ischemic stroke (IS), microglia and astrocytes undergo polarization, transforming into a pro-inflammatory phenotype (M1 or A1). According to previous studies, exosomes might play an important role in the interplay between M1 microglia and A1 astrocytes after IS. Methods: We used the microglial oxygen-glucose deprivation/reperfusion (OGD/R) model and ultracentrifugation to extract M1 microglial exosomes (M1-exos). Subsequently, we identified circSTRN3 enriched in exosomes through RNA sequencing and detected the role of circSTRN3 in astrocyte activation based on bioinformatics analysis, immunofluorescence, Western blotting, and polymerase chain reaction analysis. We validated these findings in the middle cerebral artery occlusion/reperfusion (MCAO/R) model of adult male C57BL/6J mice. Finally, we confirmed the correlation among circSTRN3, miR-331-5p, and stroke severity score in exosomes isolated from peripheral blood of IS patients. Results: Our findings revealed that M1-exos promoted A1 astrocyte activation. CircSTRN3 was abundant in M1-exos, which could sponge miR-331-5p to affect mitochondrial antiviral signaling protein (MAVS), activate NF-κB pathway, and participate in A1 astrocyte activation. In addition, overexpressed circSTRN3 augmented the infarct size and neurological dysfunction in MCAO/R models, while miR-331-5p mimics reversed the effect. Furthermore, circSTRN3 in IS patients was positively correlated with stroke severity score ( Conclusion: Taken together, our research indicated that circSTRN3 from M1-exos could promote A1 astrocyte activation and exacerbate ischemic brain injury via miR331-5p/MAVS/NF-κB axis.
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