ArticleMolecular pharmacology2011
Proinflammatory stimuli control N-acylphosphatidylethanolamine-specific phospholipase D expression in macrophages.
Article in Molecular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 84 citations in OpenAlex.
- A pilot safety, tolerability and pharmacokinetic study of an oro-buccal administered cannabidiol-dominant anti-inflammatory formulation in healthy individuals: a randomized placebo-controlled single-blinded study.Inflammopharmacology · 2021Trial
- Regulation of Cholesterol and Triglyceride Metabolism by Fatty acid Ethanolamides.Current atherosclerosis reports · 2026Review
- Investigating Properties of Palmitoylethanolamide in Physiology and Disease: Far Beyond an Anti-Inflammatory Shield.Diseases (Basel, Switzerland) · 2026Review
- NAAA-regulated lipid signaling in monocytes controls the induction of hyperalgesic priming in mice.Nature communications · 2024Article
- Expression of MUC-2, MUC-6, NAPE-PLD, IL-6 and IL-13 in Healthy and Metaplastic Bronchial Epithelium.Diseases (Basel, Switzerland) · 2022Article
- The endocannabinoid anandamide is an airway relaxant in health and disease.Nature communications · 2022Article
- Targeting NAAA counters dopamine neuron loss and symptom progression in mouse models of parkinsonism.Pharmacological research · 2022Article
- Selective measurement of NAPE-PLD activity via a PLAJournal of lipid research · 2022Article
- Multi-omics analysis reveals the metabolic regulators of duodenal low-grade inflammation in a functional dyspepsia model.Frontiers in immunology · 2022Article
- Different roles for the acyl chain and the amine leaving group in the substrate selectivity ofJournal of enzyme inhibition and medicinal chemistry · 2021Article
- The endocannabinoid system - current implications for drug development.Journal of internal medicine · 2021Review
- EngineeredInternational journal of molecular sciences · 2021Article
- Article
- Effects of orthotopic implantation of rat prostate tumour cells upon components of the N-acylethanolamine and monoacylglycerol signalling systems: an mRNA study.Scientific reports · 2020Article
- Shifting Paradigms in Allergic Contact Dermatitis: The Role of Innate Immunity.The Journal of investigative dermatology · 2020Review
- A protective role for N-acylphosphatidylethanolamine phospholipase D in 6-OHDA-induced neurodegeneration.Scientific reports · 2019Article
- Multiple endocannabinoid-mediated mechanisms in the regulation of energy homeostasis in brain and peripheral tissues.Cellular and molecular life sciences : CMLS · 2019Review
- Leptogenic effects of NAPE require activity of NAPE-hydrolyzing phospholipase D.Journal of lipid research · 2017Article
- Bile Acid Recognition by NAPE-PLD.ACS chemical biology · 2016Article
- Endogenous N-acyl taurines regulate skin wound healing.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Palmitoylethanolamide (PEA) is an endogenous lipid amide that modulates pain and inflammation by engaging peroxisome proliferator-activated receptor type-α. Here, we show that the proinflammatory bacterial endotoxin lipopolysaccharide (LPS) decreases PEA biosynthesis in RAW264.7 macrophages by suppressing the transcription of N-acylphosphatidylethanolamine-specific phospholipase D (NAPE-PLD), which catalyzes the production of PEA and other lipid amides. Using a luciferase reporter construct and chromatin immunoprecipitation, we further show that LPS treatment reduces acetylation of histone proteins bound to the NAPE-PLD promoter, an effect that is blocked by the histone deacetylase inhibitor trichostatin A. The transcription factor Sp1 is involved in regulating baseline NAPE-PLD expression but not in the transcriptional suppression induced by LPS. The ability of LPS to down-regulate PEA biosynthesis is impaired in peritoneal macrophages from mutant NAPE-PLD-deficient mice, in which PEA is produced through a compensatory mechanism distinct from NAPE-PLD. Moreover, NAPE-PLD-deficient mice fail to mount a normal inflammatory reaction in response to carrageenan administration in vivo. Our findings suggest that proinflammatory stimuli suppress NAPE-PLD expression and PEA biosynthesis in macrophages and that this effect might contribute to the inflammatory response.
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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.