ArticleFrontiers in cell and developmental biology2020
Inhibition of PDE1-B by Vinpocetine Regulates Microglial Exosomes and Polarization Through Enhancing Autophagic Flux for Neuroprotection Against Ischemic Stroke.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Exosomes in pathogenesis, diagnosis, and therapy of ischemic stroke.Frontiers in bioengineering and biotechnology · 2022Pooled it
- Vinpocetine-An "Old" Drug with a New Face: Moving Toward a Better Understanding of Its Neuroprotective Mechanism of Action.Biomolecules · 2026Review
- Recent advances in research on novel therapeutic mechanisms and strategies for exosome-based treatment of ischemic stroke.Frontiers in pharmacology · 2026Review
- A bioengineered vinpocetine- and menstrual blood stem cell-loaded neural conduit for treating peripheral nerve injury after bone fractures.Journal of materials science. Materials in medicine · 2025Article
- Microglial Autophagy and Mitophagy in Ischemic Stroke: From Dual Roles to Therapeutic Modulation.Biology · 2025Review
- Impact of Microglia-Derived Extracellular Vesicles on Resident Central Nervous System Cell Populations After Acute Brain Injury Under Various External Stimuli Conditions.Molecular neurobiology · 2025Review
- Hypothermia regulates mitophagy and apoptosis via PINK1/Parkin-VDAC 3 signaling pathway during oxygen-glucose deprivation/recovery injury.Scientific reports · 2025Article
- Novel potential neuroprotective targets for DengZhanXiXin injection in middle cerebral artery occlusion rats recommended by quantitative proteomics and simulated docking.Frontiers in neuroscience · 2025Article
- Esketamine at a Clinical Dose Attenuates Cerebral Ischemia/Reperfusion Injury by Inhibiting AKT Signaling Pathway to Facilitate Microglia M2 Polarization and Autophagy.Drug design, development and therapy · 2025Article
- The Yin and Yang of Microglia-Derived Extracellular Vesicles in CNS Injury and Diseases.Cells · 2024Review
- Exosomes: A Cellular Communication Medium That Has Multiple Effects On Brain Diseases.Molecular neurobiology · 2024Review
- Rapamycin Alleviates Neuronal Injury and Modulates Microglial Activation After Cerebral Ischemia.Molecular neurobiology · 2024Article
- PDE1B, a potential biomarker associated with tumor microenvironment and clinical prognostic significance in osteosarcoma.Scientific reports · 2024Article
- Polyphyllin I alleviates neuroinflammation after cerebral ischemia-reperfusion injury via facilitating autophagy-mediated M2 microglial polarization.Molecular medicine (Cambridge, Mass.) · 2024Article
- Hypochlorous acid derived from microglial myeloperoxidase could mediate high-mobility group box 1 release from neurons to amplify brain damage in cerebral ischemia-reperfusion injury.Journal of neuroinflammation · 2024Article
- Review
- FUS-mediated HypEVs: Neuroprotective effects against ischemic stroke.Bioactive materials · 2023Article
- Clinical Pharmacology of Vinpocetine: Properties Revisited and Introduction of a Population Pharmacokinetic Model for Its Metabolite, Apovincaminic Acid (AVA).Pharmaceutics · 2023Article
- Article
- Immunomodulation: The next target of mesenchymal stem cell-derived exosomes in the context of ischemic stroke.World journal of stem cells · 2023Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exosomes contribute to cell-cell communications. Emerging evidence has shown that microglial exosomes may play crucial role in regulation of neuronal functions under ischemic conditions. However, the underlying mechanisms of microglia-derived exosome biosynthesis are largely unknown. Herein, we reported that the microglial PDE1-B expression was progressively elevated in the peri-infarct region after focal middle cerebral artery occlusion. By an oxygen-glucose-deprivation (OGD) ischemic model in cells, we found that inhibition of PDE1-B by vinpocetine in the microglial cells promoted M2 and inhibited M1 phenotype. In addition, knockdown or inhibition of PDE1-B significantly enhanced the autophagic flux in BV2 cells, and vinpocetine-mediated suppression of M1 phenotype was dependent on autophagy in ischemic conditions. Co-culture of BV2 cells and neurons revealed that vinpocetine-treated BV2 cells alleviated OGD-induced neuronal damage, and treatment of BV2 cells with 3-MA abolished the observed effects of vinpocetine. We further demonstrated that ischemia and vinpocetine treatment significantly altered microglial exosome biogenesis and release, which could be taken up by recipient neurons and regulated neuronal damage. Finally, we showed that the isolated exosome
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