ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Suppression of inflammation with conditional deletion of the prostaglandin E2 EP2 receptor in macrophages and brain microglia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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Who cites it
63 citing papers in PubMed, 92 citations in OpenAlex.
- Prostaglandins: Key players in immunomodulation of the nervous system.Neural regeneration research · 2026Article
- Prostaglandin E2 receptor EP2 is indispensable for maintenance of skeletal muscle stem cells.Stem cells (Dayton, Ohio) · 2026Article
- Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026Review
- Capillary-Associated Microglia in Neurovascular Coupling: Localization, Mechanisms, and Disease Implications.Journal of neuroinflammation · 2026Review
- Article
- Pericytes mediate neuroinflammation via Fli-1 in endotoxemia and sepsis in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Cytomegalovirus infection of the fetal brain: intake of aspirin during pregnancy blunts neurodevelopmental pathogenesis in the offspring.Journal of neuroinflammation · 2024Article
- NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling.Nature neuroscience · 2024Article
- Strategies for Overcoming Immune Evasion in Bladder Cancer.International journal of molecular sciences · 2024Review
- Arachidonic acid-derived lipid mediators in multiple sclerosis pathogenesis: fueling or dampening disease progression?Journal of neuroinflammation · 2024Review
- Bacteroides Fragilis in the gut microbiomes of Alzheimer's disease activates microglia and triggers pathogenesis in neuronal C/EBPβ transgenic mice.Nature communications · 2023Article
- Suppression of PGE2/EP2 signaling alleviates Hirschsprung disease by upregulating p38 mitogen-activated protein kinase activity.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Prostaglandin EProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- CB1 as a novel target for Ginkgo biloba's terpene trilactone for controlling chemotherapy-induced peripheral neuropathy (CIPN).Journal of molecular modeling · 2022Article
- Cerebral dysfunctions caused by sepsis during ageing.Nature reviews. Immunology · 2022Review
- Group 3 innate lymphoid cells produce the growth factor HB-EGF to protect the intestine from TNF-mediated inflammation.Nature immunology · 2022Article
- Sepsis-Associated Encephalopathy: A Mini-Review of Inflammation in the Brain and Body.Frontiers in aging neuroscience · 2022Review
- EP2 Antagonists (2011-2021): A Decade's Journey from Discovery to Therapeutics.Journal of medicinal chemistry · 2021Review
- A PGEImmunity · 2021Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Prostaglandin E2 (PGE2), a potent lipid signaling molecule, modulates inflammatory responses through activation of downstream G-protein coupled EP(1-4) receptors. Here, we investigated the cell-specific in vivo function of PGE2 signaling through its E-prostanoid 2 (EP2) receptor in murine innate immune responses systemically and in the CNS. In vivo, systemic administration of lipopolysaccharide (LPS) resulted in a broad induction of cytokines and chemokines in plasma that was significantly attenuated in EP2-deficient mice. Ex vivo stimulation of peritoneal macrophages with LPS elicited proinflammatory responses that were dependent on EP2 signaling and that overlapped with in vivo plasma findings, suggesting that myeloid-lineage EP2 signaling is a major effector of innate immune responses. Conditional deletion of the EP2 receptor in myeloid lineage cells in Cd11bCre;EP2(lox/lox) mice attenuated plasma inflammatory responses and transmission of systemic inflammation to the brain was inhibited, with decreased hippocampal inflammatory gene expression and cerebral cortical levels of IL-6. Conditional deletion of EP2 significantly blunted microglial and astrocytic inflammatory responses to the neurotoxin MPTP and reduced striatal dopamine turnover. Suppression of microglial EP2 signaling also increased numbers of dopaminergic (DA) neurons in the substantia nigra independent of MPTP treatment, suggesting that microglial EP2 may influence development or survival of DA neurons. Unbiased microarray analysis of microglia isolated from adult Cd11bCre;EP2(lox/lox) and control mice demonstrated a broad downregulation of inflammatory pathways with ablation of microglial EP2 receptor. Together, these data identify a cell-specific proinflammatory role for macrophage/microglial EP2 signaling in innate immune responses systemically and in brain.
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Registered trials
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.