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ABSTRACT: Background and purpose
Endocannabinoids 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 results
AEA pretreatment attenuated the cytokine-m
SUBMITTER: Teichmann T
PROVIDER: S-EPMC11790392 | biostudies-literature | 2025 Mar
REPOSITORIES: biostudies-literature