ArticleNeurotoxicology2011
Manganese potentiates LPS-induced heme-oxygenase 1 in microglia but not dopaminergic cells: role in controlling microglial hydrogen peroxide and inflammatory cytokine output.
Article in Neurotoxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Combined Manganese-Iron Exposure Reduced Oxidative Stress is Associated with the NRF2/NQO1 Pathway in Astrocytic C8-D1A Cells.Biological trace element research · 2026Article
- Article
- Behavioral Alterations in Mice Exposed to Manganese via Drinking Water: Effects of Sex and a Lipopolysaccharide Challenge.Journal of applied toxicology : JAT · 2025Article
- Divalent Metal Uptake and the Role of ZIP8 in Host Defense Against Pathogens.Frontiers in cell and developmental biology · 2022Review
- Crosstalk between Neuron and Glial Cells in Oxidative Injury and Neuroprotection.International journal of molecular sciences · 2021Review
- Mechanism of Gene-Environment Interactions Driving Glial Activation in Parkinson's Diseases.Current environmental health reports · 2021Review
- Optimal Level of Supplemental Manganese for Yellow-Feathered Broilers during the Growth Phase.Animals : an open access journal from MDPI · 2021Article
- Neurotoxicity mechanisms of manganese in the central nervous system.Advances in neurotoxicology · 2021Article
- Manganese Accumulation in the Brain via Various Transporters and Its Neurotoxicity Mechanisms.Molecules (Basel, Switzerland) · 2020Review
- Astaxanthin Suppresses PM2.5-Induced Neuroinflammation by Regulating Akt Phosphorylation in BV-2 Microglial Cells.International journal of molecular sciences · 2020Article
- Environmental neurotoxicant-induced dopaminergic neurodegeneration: a potential link to impaired neuroinflammatory mechanisms.Pharmacology & therapeutics · 2019Review
- Manganese activates NLRP3 inflammasome signaling and propagates exosomal release of ASC in microglial cells.Science signaling · 2019Article
- The Impact of Dietary Transition Metals on Host-Bacterial Interactions.Cell host & microbe · 2018Review
- RNA-binding protein Lin28 is associated with injured dentin-dental pulp complex in Sprague-Dawley rats.International journal of clinical and experimental pathology · 2018Article
- The effect of manganese nanoparticles on apoptosis and on redox and immune status in the tissues of young turkeys.PloS one · 2018Article
- Investigation of manganese homeostasis in dogs with anaemia and chronic enteropathy.Open veterinary journal · 2017Article
- Behavioral and monoamine perturbations in adult male mice with chronic inflammation induced by repeated peripheral lipopolysaccharide administration.Behavioural brain research · 2016Article
- Mechanisms of divalent metal toxicity in affective disorders.Toxicology · 2016Review
- Interleukin-10 Protection against Lipopolysaccharide-Induced Neuro-Inflammation and Neurotoxicity in Ventral Mesencephalic Cultures.International journal of molecular sciences · 2015Article
- Molecular mechanisms of lipopolysaccharide-mediated inhibition of glutathione synthesis in mice.Free radical biology & medicine · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Excessive manganese (Mn) exposure increases output of glial-derived inflammatory products, which may indirectly contribute to the neurotoxic effects of this essential metal. In microglia, Mn increases hydrogen peroxide (H(2)O(2)) release and potentiates lipopolysaccharide (LPS)-induced cytokines (TNF-α, IL-6) and nitric oxide (NO). Inducible heme-oxygenase (HO-1) plays a role in the regulation of inflammation and its expression is upregulated in response to oxidative stressors, including metals and LPS. Because Mn can oxidatively affect neurons both directly and indirectly, we investigated the effect of Mn exposure on the induction of HO-1 in resting and LPS-activated microglia (N9) and dopaminergic neurons (N27). In microglia, 24h exposure to Mn (up to 250 μM) had minimal effects on its own, but it markedly potentiated LPS (100 ng/ml)-induced HO-1 protein and mRNA. Inhibition of microglial HO-1 activity with two different inhibitors indicated that HO-1 is a positive regulator of the Mn-potentiated cytokine output and a negative regulator of the Mn-induced H(2)O(2) output. Mn enhancement of LPS-induced HO-1 does not appear to be dependent on H(2)O(2) or NO, as Mn+LPS-induced H(2)O(2) release was not greater than the increase induced by Mn alone and inhibition of iNOS did not change Mn potentiation of HO-1. However, because Mn exposure potentiated the LPS-induced nuclear expression of small Maf proteins, this may be one mechanism Mn uses to affect the expression of HO-1 in activated microglia. Finally, the potentiating effects of Mn on HO-1 appear to be glia-specific for Mn, LPS, or Mn+LPS did not induce HO-1 in N27 neuronal cells.
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Registered trials
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