ArticleBritish journal of pharmacology2010
Endocannabinoid-like N-arachidonoyl serine is a novel pro-angiogenic mediator.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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.
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Who cites it
45 citing papers in PubMed, 94 citations in OpenAlex.
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- GPR55-mediated effects on brain microvascular endothelial cells and the blood-brain barrier.Neuroscience · 2019Article
- Activation of GPR55 increases neural stem cell proliferation and promotes early adult hippocampal neurogenesis.British journal of pharmacology · 2018Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
background and purposeN-arachidonoyl serine (ARA-S) is a recently identified endocannabinoid-like lipid with weak affinity for the fully characterized cannabinoid receptors (CB(1) and CB(2)) and the transient receptor potential vanilloid receptor 1 (TRPV-1). ARA-S induces vasodilatation and shows vasoprotective potential via activation of key signalling pathways in endothelial cells. Based on these findings, the effect of ARA-S on endothelial functions was further studied. EXPERIMENTAL APPROACH: Primary human dermal microvascular endothelial cells (HMVEC) were used to investigate effects of ARA-S (0-10 microM) on certain endothelial functions, using cell proliferation, migration and wound repair models in vitro, and angiogenesis assays in vitro and ex vivo. Selective CB receptor antagonists and specific siRNAs were deployed to block individual CB receptors. KEY
resultsWe found that ARA-S stimulated angiogenesis and endothelial wound healing through induction of vascular endothelial growth factor C and its cognate receptor expression in primary HMVEC. Moreover, knock-down of G protein-coupled receptor 55 (GPR55) partly inhibited ARA-S-induced signal transduction and endothelial functions. CONCLUSIONS AND IMPLICATIONS: Our results indicate that ARA-S is a pro-angiogenic factor in addition to a vessel dilator. The GPR55 receptor may serve as one target of ARA-S.
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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.