ArticlePloS one2013
Astrocytes protect neurons against methylmercury via ATP/P2Y(1) receptor-mediated pathways in astrocytes.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Nrf2 and STAT3 Pathways in Protecting Against Methylmercury-Induced Oxidative Stress in Hypothalamic Neuronal GT1-7 Cells.Neurochemical research · 2026Article
- Exploring neuroglial signaling: diversity of molecules implicated in microglia-to-astrocyte neuroimmune communication.Reviews in the neurosciences · 2025Review
- Characterization of pathological changes in the olfactory system of mice exposed to methylmercury.Archives of toxicology · 2024Article
- Astrocyte Immune Functions and Glaucoma.International journal of molecular sciences · 2023Review
- Unraveling molecular characteristic of fluoride neurotoxicity on U87 glial-like cells: insights from transcriptomic and proteomic approach.Frontiers in cellular neuroscience · 2023Article
- Sex-related differences in the response of anti-platelet drug therapies targeting purinergic signaling pathways in sepsis.Frontiers in immunology · 2022Article
- Revisiting Astrocytic Roles in Methylmercury Intoxication.Molecular neurobiology · 2021Review
- Methylmercury induces neuronal cell death by inducing TNF-α expression through the ASK1/p38 signaling pathway in microglia.Scientific reports · 2021Article
- Cellular and Molecular Mechanisms Mediating Methylmercury Neurotoxicity and Neuroinflammation.International journal of molecular sciences · 2021Review
- Neurotoxicity of mercury: an old issue with contemporary significance.Advances in neurotoxicology · 2021Article
- Neuroprotective effects of microglial P2YJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Neuroprotective activation of astrocytes by methylmercury exposure in the inferior colliculus.Scientific reports · 2019Article
- Post-translational modifications in MeHg-induced neurotoxicity.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Vascular Dysfunction Induced by Mercury Exposure.International journal of molecular sciences · 2019Review
- Chemokine CCL4 Induced in Mouse Brain Has a Protective Role against Methylmercury Toxicity.Toxics · 2018Article
- Article
- Oral Delivery of a Synthetic Sterol Reduces Axonopathy and Inflammation in a Rodent Model of Glaucoma.Frontiers in neuroscience · 2017Article
- Methylmercury induces the expression of TNF-α selectively in the brain of mice.Scientific reports · 2016Article
- Tea Polyphenols Protect Against Methylmercury-Induced Cell Injury in Rat Primary Cultured Astrocytes, Involvement of Oxidative Stress and Glutamate Uptake/Metabolism Disorders.Molecular neurobiology · 2016Article
- Cell-permeable p38 MAP kinase promotes migration of adult neural stem/progenitor cells.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylmercury (MeHg) is a well known environmental pollutant that induces serious neuronal damage. Although MeHg readily crosses the blood-brain barrier, and should affect both neurons and glial cells, how it affects glia or neuron-to-glia interactions has received only limited attention. Here, we report that MeHg triggers ATP/P2Y1 receptor signals in astrocytes, thereby protecting neurons against MeHg via interleukin-6 (IL-6)-mediated pathways. MeHg increased several mRNAs in astrocytes, among which IL-6 was the highest. For this, ATP/P2Y1 receptor-mediated mechanisms were required because the IL-6 production was (i) inhibited by a P2Y1 receptor antagonist, MRS2179, (ii) abolished in astrocytes obtained from P2Y1 receptor-knockout mice, and (iii) mimicked by exogenously applied ATP. In addition, (iv) MeHg released ATP by exocytosis from astrocytes. As for the intracellular mechanisms responsible for IL-6 production, p38 MAP kinase was involved. MeHg-treated astrocyte-conditioned medium (ACM) showed neuro-protective effects against MeHg, which was blocked by anti-IL-6 antibody and was mimicked by the application of recombinant IL-6. As for the mechanism of neuro-protection by IL-6, an adenosine A1 receptor-mediated pathway in neurons seems to be involved. Taken together, when astrocytes sense MeHg, they release ATP that autostimulates P2Y1 receptors to upregulate IL-6, thereby leading to A1 receptor-mediated neuro-protection against MeHg.
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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.