ArticleBasic research in cardiology2020
The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells.
Article in Basic research in cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Targeting B7-H3 attenuates uremic vascular calcification by suppressing phenotypic switching of VSMCs and regulating VSMCs-macrophage crosstalk.Clinical and experimental nephrology · 2026Article
- Immune cell exhaustion and apoptotic markers in major depressive disorder: Effects of in vitro cannabidiol administration.Brain, behavior, & immunity - health · 2025Article
- The endocannabinoid anandamide mediates anti-inflammatory effects through activation of NR4A nuclear receptors.British journal of pharmacology · 2025Article
- FGF2 Attenuated Inflammation-Mediated Cardiac Damage: A Novel Mechanistic Insight into the AMPK-FUNDC1-Mitophagy.Research (Washington, D.C.) · 2025Article
- Epigenetic regulation-mediated disorders in dopamine transporter endocytosis: A novel mechanism for the pathogenesis of Parkinson's disease.Theranostics · 2025Review
- The platelet and plasma proteome and targeted lipidome in postpartum dairy cows with elevated systemic inflammation.Scientific reports · 2024Article
- The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses.Frontiers in pharmacology · 2024Article
- A zebrafish HCT116 xenograft model to predict anandamide outcomes on colorectal cancer.Cell death & disease · 2022Article
- Non-psychotropic Cannabis sativa L. phytocomplex modulates microglial inflammatory response through CB2 receptors-, endocannabinoids-, and NF-κB-mediated signaling.Phytotherapy research : PTR · 2022Article
- Mitophagy alleviates ischemia/reperfusion-induced microvascular damage through improving mitochondrial quality control.Bioengineered · 2022Article
- Abnormal Mitochondria-Endoplasmic Reticulum Communication Promotes Myocardial Infarction.Frontiers in physiology · 2021Article
- Mitofusin-2 Enhances Mitochondrial Contact With the Endoplasmic Reticulum and Promotes Diabetic Cardiomyopathy.Frontiers in physiology · 2021Article
- Protective Effect of Nicorandil on Cardiac Microvascular Injury: Role of Mitochondrial Integrity.Oxidative medicine and cellular longevity · 2021Review
- Overexpression of SERCA2a Alleviates Cardiac Microvascular Ischemic Injury by Suppressing Mfn2-Mediated ER/Mitochondrial Calcium Tethering.Frontiers in cell and developmental biology · 2021Article
- Molecular Perspectives of Mitophagy in Myocardial Stress: Pathophysiology and Therapeutic Targets.Frontiers in physiology · 2021Review
- Melatonin Attenuates Cardiac Ischemia-Reperfusion Injury through Modulation of IP3R-Mediated Mitochondria-ER Contact.Oxidative medicine and cellular longevity · 2021Article
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endocannabinoids are important lipid-signaling mediators. Both protective and deleterious effects of endocannabinoids in the cardiovascular system have been reported but the mechanistic basis for these contradicting observations is unclear. We set out to identify anti-inflammatory mechanisms of endocannabinoids in the murine aorta and in human vascular smooth muscle cells (hVSMC). In response to combined stimulation with cytokines, IL-1β and TNFα, the murine aorta released several endocannabinoids, with anandamide (AEA) levels being the most significantly increased. AEA pretreatment had profound effects on cytokine-induced gene expression in hVSMC and murine aorta. As revealed by RNA-Seq analysis, the induction of a subset of 21 inflammatory target genes, including the important cytokine CCL2 was blocked by AEA. This effect was not mediated through AEA-dependent interference of the AP-1 or NF-κB pathways but rather through an epigenetic mechanism. In the presence of AEA, ATAC-Seq analysis and chromatin-immunoprecipitations revealed that CCL2 induction was blocked due to increased levels of H3K27me3 and a decrease of H3K27ac leading to compacted chromatin structure in the CCL2 promoter. These effects were mediated by recruitment of HDAC4 and the nuclear corepressor NCoR1 to the CCL2 promoter. This study therefore establishes a novel anti-inflammatory mechanism for the endogenous endocannabinoid AEA in vascular smooth muscle cells. Furthermore, this work provides a link between endogenous endocannabinoid signaling and epigenetic regulation.
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