ArticleBritish journal of pharmacology2025
The endocannabinoid anandamide mediates anti-inflammatory effects through activation of NR4A nuclear receptors.
Article in British journal of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Transcriptomic and functional responses of human airway cells to vaped ∆8-THC and its oxidation product ∆8-THCQ.Scientific reports · 2026Article
- Comparative Lipidomic Profiling of Camel and Cow Milk from a Shared Semi-Desert Pasture: Implications for Camel Adaptation to Arid Environments.Molecules (Basel, Switzerland) · 2026Article
- Recent Change in Anhedonia, Major Depression and Low-Grade Inflammation: Dangerous Liaisons? A Study Based on a Cohort Referred for Polysomnography.Medicina (Kaunas, Lithuania) · 2025Article
- The Endocannabinoid-Microbiota-Neuroimmune Super-System: A Unifying Feedback Architecture for Systems Resilience, Collapse Trajectories, and Precision Feedback Medicine.International journal of molecular sciences · 2025Review
- Oxylipins in Atherosclerosis: Their Role in Inflammation, Diagnosis, and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
- Review
- The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses.Frontiers in pharmacology · 2024Article
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Authors and funding
26 authors.
Funding
Abstract
background and purposeEndocannabinoids are lipid mediators, which elicit complex biological effects that extend beyond the central nervous system. Tissue concentrations of endocannabinoids increase in atherosclerosis, and for the endocannabinoid N-arachidonoyl-ethanolamine (anandamide, AEA), this has been linked to an anti-inflammatory function. In this study, we set out to determine the anti-inflammatory mechanism of action of AEA, specifically focusing on vascular smooth muscle cells. EXPERIMENTAL APPROACH: RNA-sequencing, RT-qPCR, LC-MS/MS, NanoBit, ChIP, microscale thermophoresis, NMR structural footprinting, Gal4 reporter gene assays and loss of function approaches in cell and ex vivo organ culture were used. KEY
resultsAEA pretreatment attenuated the cytokine-mediated induction of inflammatory gene expression such as CCL2. This effect was also observed in preparations obtained from cannabinoid receptor knockout mice and after pertussis toxin treatment. The anti-inflammatory effect of AEA required preincubation, suggesting an effect through gene induction. AEA increased the expression of the nuclear receptors NR4A1 and NR4A2. Knockdown and knockout of these receptors blocked the AEA-mediated anti-inflammatory effect in cell culture and aortic organ culture, respectively. Conversely, NR4A agonists (CsnB, C-DIM12) attenuated inflammatory gene expression. AEA binds to NR4A, and mutations in NR4A attenuated this effect. The interaction of AEA with NR4A caused recruitment of the nuclear corepressor NCoR1 to the CCL2 promoter, resulting in gene suppression. CONCLUSION AND IMPLICATIONS: By binding to NR4A, AEA elicits an anti-inflammatory response in vascular smooth muscle cells. NR4A-binding by AEA analogues may represent novel anti-inflammatory agents.
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