ArticleThe Journal of biological chemistry2011
Anti-inflammatory role of microsomal prostaglandin E synthase-1 in a model of neuroinflammation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 77 citations in OpenAlex.
- Convergence of sepsis-associated encephalopathy pathogenesis onto microglia.Journal of translational medicine · 2025Review
- Spatial mapping of the AA-PGEActa neuropathologica · 2025Article
- Prostaglandins in the Inflamed Central Nervous System: Potential Therapeutic Targets.Current drug targets · 2024Review
- Update on the pathological roles of prostaglandin ETranslational neurodegeneration · 2023Review
- SILAC-based quantitative proteomics to investigate the eicosanoid associated inflammatory response in activated macrophages.Journal of inflammation (London, England) · 2022Article
- Re-Expression of Tafazzin Isoforms in TAZ-Deficient C6 Glioma Cells Restores Cardiolipin Composition but Not Proliferation Rate and Alterations in Gene Expression.Frontiers in genetics · 2022Article
- Prostanoids and Resolution of Inflammation - Beyond the Lipid-Mediator Class Switch.Frontiers in immunology · 2021Review
- Sulforaphene Ameliorates Neuroinflammation and Hyperphosphorylated Tau Protein via Regulating the PI3K/Akt/GSK-3Oxidative medicine and cellular longevity · 2020Article
- Prostaglandins as the Agents That Modulate the Course of Brain Disorders.Degenerative neurological and neuromuscular disease · 2020Review
- Pharmacological plasticity-How do you hit a moving target?Pharmacology research & perspectives · 2019Review
- Augmented liver inflammation in a microsomal prostaglandin E synthase 1 (mPGES-1)-deficient diet-induced mouse NASH model.Scientific reports · 2018Article
- Effect of PGEOncotarget · 2017Article
- Differential expression of E-type prostanoid receptors 2 and 4 in microglia stimulated with lipopolysaccharide.Journal of neuroinflammation · 2017Article
- Statins Reduce Lipopolysaccharide-Induced Cytokine and Inflammatory Mediator Release in an In Vitro Model of Microglial-Like Cells.Mediators of inflammation · 2017Article
- Antinociceptive effect of a novel armed spider peptide Tx3-5 in pathological pain models in mice.Pflugers Archiv : European journal of physiology · 2016Article
- Misoprostol Reverse Hippocampal Neuron Cyclooxygenase-2 Downstream Signaling Imbalance in Aluminum-Overload Rats.Current Alzheimer research · 2016Article
- MPGES-1-derived PGE2 suppresses CD80 expression on tumor-associated phagocytes to inhibit anti-tumor immune responses in breast cancer.Oncotarget · 2015Article
- Neuroinflammation in Alzheimer's disease.The Lancet. Neurology · 2015Review
- Transgenic increase in n-3/n-6 fatty acid ratio protects against cognitive deficits induced by an immune challenge through decrease of neuroinflammation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Gene expression profile of compressed primary human cementoblasts before and after IL-1β stimulation.Clinical oral investigations · 2014Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major immunological response during neuroinflammation is the activation of microglia, which subsequently release proinflammatory mediators such as prostaglandin E(2) (PGE(2)). Besides its proinflammatory properties, cyclooxygenase-2 (COX-2)-derived PGE(2) has been shown to exhibit anti-inflammatory effects on innate immune responses. Here, we investigated the role of microsomal PGE(2) synthase-1 (mPGES-1), which is functionally coupled to COX-2, in immune responses using a model of lipopolysaccharide (LPS)-induced spinal neuroinflammation. Interestingly, we found that activation of E-prostanoid (EP)2 and EP4 receptors, but not EP1, EP3, PGI(2) receptor (IP), thromboxane A(2) receptor (TP), PGD(2) receptor (DP), and PGF(2) receptor (FP), efficiently blocked LPS-induced tumor necrosis factor α (TNFα) synthesis and COX-2 and mPGES-1 induction as well as prostaglandin synthesis in spinal cultures. In vivo, spinal EP2 receptors were up-regulated in microglia in response to intrathecally injected LPS. Accordingly, LPS priming reduced spinal synthesis of TNFα, interleukin 1β (IL-1β), and prostaglandins in response to a second intrathecal LPS injection. Importantly, this reduction was only seen in wild-type but not in mPGES-1-deficient mice. Furthermore, intrathecal application of EP2 and EP4 agonists as well as genetic deletion of EP2 significantly reduced spinal TNFα and IL-1β synthesis in mPGES-1 knock-out mice after LPS priming. These data suggest that initial inflammation prepares the spinal cord for a negative feedback regulation by mPGES-1-derived PGE(2) followed by EP2 activation, which limits the synthesis of inflammatory mediators during chronic inflammation. Thus, our data suggest a role of mPGES-1-derived PGE(2) in resolution of neuroinflammation.
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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.