ArticleJournal of neuroinflammation2017
Agonists for G-protein-coupled receptor 84 (GPR84) alter cellular morphology and motility but do not induce pro-inflammatory responses in microglia.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- GPR84 and Neuroinflammation: A Receptor Worth Targeting, or A Target Worth Reconsidering?Molecular neurobiology · 2026Review
- Itaconic Acid: A Regulator of Immune Responses and Inflammatory Metabolism.Current issues in molecular biology · 2025Review
- G-Protein-Coupled Receptor 84 Aggravates Early Brain Injury via Microglial NLRP3-ASC Inflammasome After Subarachnoid Hemorrhage.Brain and behavior · 2025Article
- Synthetic GPR84 Agonists in Colorectal Cancer: Effective in THP-1 Cells but Ineffective in BMDMs and MC38 Mouse Tumor Models.International journal of molecular sciences · 2025Article
- Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages.Microorganisms · 2025Article
- Single-Cell RNA Sequencing Reveals Microglial Heterogeneity and Functional States After Cerebral Ischemia-Reperfusion Injury.Journal of inflammation research · 2025Article
- G-protein-coupled receptor 84 regulates acute inflammation in normal and diabetic skin wounds.Cell reports · 2024Article
- Systematic characterization of multi-omics landscape between gut microbial metabolites and GPCRome in Alzheimer's disease.Cell reports · 2024Article
- The role of orphan G protein-coupled receptors in pain.Heliyon · 2024Review
- Exploring orphan GPCRs in neurodegenerative diseases.Frontiers in pharmacology · 2024Review
- Investigating the causal effect of various metabolites on postherpetic neuralgia: a Mendelian randomization study.Frontiers in neurology · 2024Article
- Molecular Cloning, Tissue Distribution, and Pharmacological Characterization of GPR84 in Grass Carp (Animals : an open access journal from MDPI · 2023Article
- Pro-phagocytic function and structural basis of GPR84 signaling.Nature communications · 2023Article
- Lipopolysaccharide Preconditioning Restricts Microglial Overactivation and Alleviates Inflammation-Induced Depressive-like Behavior in Mice.Brain sciences · 2023Article
- Pro-phagocytic function and structural basis of GPR84 signaling.Research square · 2023Article
- Type 2 diabetes is associated with increased circulating levels of 3-hydroxydecanoate activating GPR84 and neutrophil migration.iScience · 2022Article
- Therapeutic validation of an orphan G protein-coupled receptor: The case of GPR84.British journal of pharmacology · 2022Review
- Dietary Medium-Chain Triglyceride Decanoate Affects Glucose Homeostasis Through GPR84-Mediated GLP-1 Secretion in Mice.Frontiers in nutrition · 2022Article
- Discovery and Characterization of Novel Antagonists of the Proinflammatory Orphan Receptor GPR84.ACS pharmacology & translational science · 2021Article
- GPR84 Is Essential for the Taste of Medium Chain Saturated Fatty Acids.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSeveral G-protein-coupled receptors (GPCRs) have been shown to be important signaling mediators between neurons and glia. In our previous screening for identification of nerve injury-associated GPCRs, G-protein-coupled receptor 84 (GPR84) mRNA showed the highest up-regulation by microglia after nerve injury. GPR84 is a pro-inflammatory receptor of macrophages in a neuropathic pain mouse model, yet its function in resident microglia in the central nervous system is poorly understood.
methodsWe used endogenous, natural, and surrogate agonists for GPR84 (capric acid, embelin, and 6-OAU, respectively) and examined their effect on mouse primary cultured microglia in vitro.
results6-n-Octylaminouracil (6-OAU), embelin, and capric acid rapidly induced membrane ruffling and motility in cultured microglia obtained from C57BL/6 mice, although these agonists failed to promote microglial pro-inflammatory cytokine expression. Concomitantly, 6-OAU suppressed forskolin-induced increase of cAMP in cultured microglia. Pertussis toxin, an inhibitor of Gi-coupled signaling, completely suppressed 6-OAU-induced microglial membrane ruffling and motility. In contrast, no 6-OAU-induced microglial membrane ruffling and motility was observed in microglia from DBA/2 mice, a mouse strain that does not express functional GPR84 protein due to endogenous nonsense mutation of the GPR84 gene.
conclusionsGPR84 mediated signaling causes microglial motility and membrane ruffling but does not promote pro-inflammatory responses. As GPR84 is a known receptor for medium-chain fatty acids, those released from damaged brain cells may be involved in the enhancement of microglial motility through GPR84 after neuronal injury.
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