ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
The role of G-protein receptor 84 in experimental neuropathic pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 66 citations in OpenAlex.
- Orphan GPR84 facilitates uropod de-adhesion at multiple steps during leukocyte extravasation.EMBO reports · 2026Article
- Pharmacological modulation of GPR84 revealed by dual states structures and immune functional assays.Experimental & molecular medicine · 2026Article
- GPR84 and Neuroinflammation: A Receptor Worth Targeting, or A Target Worth Reconsidering?Molecular neurobiology · 2026Review
- Gnao1 acts as a gatekeeper to alleviate neuropathic pain by silencing pro-nociceptive signaling cascades.The journal of headache and pain · 2026Article
- Fatty Acid-Sensing G Protein-Coupled Receptors in Skeletal Metabolism.Journal of bone metabolism · 2026Article
- Agonism of GPR84 Attenuates Free Fatty Acid-Induced Endothelial Inflammation and Monocyte Adhesion via Gfi1/NF-κB Pathway.Arquivos brasileiros de cardiologia · 2026Article
- The role of the gut microbiota in the development of rheumatic diseases: a focus on fibromyalgia.Frontiers in immunology · 2026Review
- Stage-specific transcriptomic alterations in the spinal cord reveal key regulatory genes and potential therapeutic targets in a rat model of neuropathic pain.Journal of translational medicine · 2025Article
- Electroacupuncture combined with subanesthetic alfaxalone as a novel target for alleviating neuropathic pain.Pain reports · 2025Article
- Emerging role of macrophages in neuropathic pain.Journal of orthopaedic translation · 2025Review
- Human AKR1C3 binds agonists of GPR84 and participates in an expanded polyamine pathway.Cell chemical biology · 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
- Static Magnetic Stimulation and Magnetic Microwires Synergistically Enhance and Guide Neurite Outgrowth.Advanced healthcare materials · 2025Article
- Histone modifications and Sp1 promote GPR160 expression in bone cancer pain within rodent models.EMBO reports · 2024Article
- G-protein-coupled receptor 84 regulates acute inflammation in normal and diabetic skin wounds.Cell reports · 2024Article
- The role of orphan G protein-coupled receptors in pain.Heliyon · 2024Review
- Temporal changes of spinal microglia in murine models of neuropathic pain: a scoping review.Frontiers in immunology · 2024Article
- PET Imaging of Innate Immune Activation UsingJACS Au · 2023Article
- GPR84 regulates pulmonary inflammation by modulating neutrophil functions.Acta pharmacologica Sinica · 2023Article
- Fatty Acid Sensing in the Gastrointestinal Tract of Rainbow Trout: Different to Mammalian Model?International journal of molecular sciences · 2023Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
G-protein receptor 84 (GPR84) is an orphan receptor that is induced markedly in monocytes/macrophages and microglia during inflammation, but its pathophysiological function is unknown. Here, we investigate the role of GPR84 in a murine model of traumatic nerve injury. Naive GPR84 knock-out (KO) mice exhibited normal behavioral responses to acute noxious stimuli, but subsequent to partial sciatic nerve ligation (PNL), KOs did not develop mechanical or thermal hypersensitivity, in contrast to wild-type (WT) littermates. Nerve injury increased ionized calcium binding adapter molecule 1 (Iba1) and phosphorylated p38 MAPK immunoreactivity in the dorsal horn and Iba1 and cluster of differentiation 45 expression in the sciatic nerve, with no difference between genotypes. PCR array analysis revealed that Gpr84 expression was upregulated in the spinal cord and sciatic nerve of WT mice. In addition, the expression of arginase-1, a marker for anti-inflammatory macrophages, was upregulated in KO sciatic nerve. Based on this evidence, we investigated whether peripheral macrophages behave differently in the absence of GPR84. We found that lipopolysaccharide-stimulated KO macrophages exhibited attenuated expression of several proinflammatory mediators, including IL-1β, IL-6, and TNF-α. Forskolin-stimulated KO macrophages also showed greater cAMP induction, a second messenger associated with immunosuppression. In summary, our results demonstrate that GPR84 is a proinflammatory receptor that contributes to nociceptive signaling via the modulation of macrophages, whereas in its absence the response of these cells to an inflammatory insult is impaired.
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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.