ArticleFrontiers in pharmacology2017
Shedding of Microvesicles from Microglia Contributes to the Effects Induced by Metabotropic Glutamate Receptor 5 Activation on Neuronal Death.
Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Enhanced exosome secretion regulated by microglial P2X7R in the medullary dorsal horn contributes to pulpitis-induced pain.Cell & bioscience · 2025Article
- Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson's Disease Model by Alleviating Mitochondrial Dysfunction.International journal of molecular sciences · 2023Article
- The Physio-Pathological Role of Group I Metabotropic Glutamate Receptors Expressed by Microglia in Health and Disease with a Focus on Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- Extracellular vesicles and Alzheimer's disease in the novel era of Precision Medicine: implications for disease progression, diagnosis and treatment.Experimental neurology · 2022Review
- Neuroprotective and Neurotoxic Effects of Glial-Derived Exosomes.Frontiers in cellular neuroscience · 2022Review
- Cytokine Signalling at the Microglial Penta-Partite Synapse.International journal of molecular sciences · 2021Review
- Extracellular Vesicles and HIV-Associated Neurocognitive Disorders: Implications in Neuropathogenesis and Disease Diagnosis.Neurotoxicity research · 2021Review
- Role of G Protein-Coupled Receptors in Microglial Activation: Implication in Parkinson's Disease.Frontiers in aging neuroscience · 2021Review
- Extracellular Vesicles as a Means of Viral Immune Evasion, CNS Invasion, and Glia-Induced Neurodegeneration.Frontiers in cellular neuroscience · 2021Article
- Glia-Derived Extracellular Vesicles: Role in Central Nervous System Communication in Health and Disease.Frontiers in cell and developmental biology · 2020Review
- Insights Into the Proteomic Profiling of Extracellular Vesicles for the Identification of Early Biomarkers of Neurodegeneration.Frontiers in neurology · 2020Review
- The Ambiguous Role of Microglia in Aβ Toxicity: Chances for Therapeutic Intervention.Current neuropharmacology · 2020Review
- Neutral Sphingomyelinase Inhibition Alleviates LPS-Induced Microglia Activation and Neuroinflammation after Experimental Traumatic Brain Injury.The Journal of pharmacology and experimental therapeutics · 2019Article
- Metabotropic Glutamate Receptors in Glial Cells: A New Potential Target for Neuroprotection?Frontiers in molecular neuroscience · 2018Review
- Importance of GPCR-Mediated Microglial Activation in Alzheimer's Disease.Frontiers in cellular neuroscience · 2018Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabotropic glutamate (mGlu) receptor 5 is involved in neuroinflammation and has been shown to mediate reduced inflammation and neurotoxicity and to modify microglia polarization. On the other hand, blockade of mGlu5 receptor results in inhibition of microglia activation. To dissect this controversy, we investigated whether microvesicles (MVs) released from microglia BV2 cells could contribute to the communication between microglia and neurons and whether this interaction was modulated by mGlu5 receptor. Activation of purinergic ionotropic P2X7 receptor with the stable ATP analog benzoyl-ATP (100 μM) caused rapid MVs shedding from BV2 cells. Ionic currents through P2X7 receptor increased in BV2 cells pretreated for 24 h with the mGlu5 receptor agonist CHPG (200 μM) as by patch-clamp recording. This increase was blunted when microglia cells were activated by exposure to lipopolysaccharide (LPS; 0.1 μg/ml for 6 h). Accordingly, a greater amount of MVs formed after CHPG treatment, an effect prevented by the mGlu5 receptor antagonist MTEP (100 μM), as measured by expression of flotillin, a membrane protein enriched in MVs. Transferred MVs were internalized by SH-SY5Y neurons where they did not modify neuronal death induced by a low concentration of rotenone (0.1 μM for 24 h), but significantly increased rotenone neurotoxicity when shed from CHPG-treated BV2 cells. miR146a was increased in CHPG-treated MVs, an effect concealed in MVs from LPS-activated BV2 cells that showed
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