Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA)
Regular ArticleOxidative metabolism of endocannabinoids☆
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New role for the anandamide metabolite prostaglandin F<inf>2α</inf> ethanolamide: Rolling preadipocyte proliferation
2023, Journal of Lipid ResearchEicosanoid mediation of cannabinoid actions
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2017, Advances in PharmacologyCitation Excerpt :Similarly, it has been demonstrated that 2-AG can be selectively oxygenated by this enzyme. The oxygenation of eCBs by COX-2 leads to the formation of prostaglandin-ethanolamides (prostamides, PMs) and prostaglandin-glyceryl esters with unique pharmacological properties (Fig. 4; Kozak & Marnett, 2002). COX-2 oxygenates AEA first to PGH2-ethanolamide, which, probably through the action of prostaglandin E synthase, is then converted PGE2-ethanolamide (PME2), the first prostamide to be discovered (Yu, Ives, & Ramesha, 1997).
Cyclooxygenase-2 contributes to the selective induction of cell death by the endocannabinoid 2-arachidonoyl glycerol in hepatic stellate cells
2016, Biochemical and Biophysical Research CommunicationsCitation Excerpt :It was recently shown that 2-AG is first metabolized by COX-2 to unstable PGH2-GE. PGH2-GE acts as a substrate for PGD-, PGE- or PGF-synthases resulting in PGD2-GE, PGE2-GE or PGF2α-GE, respectively [24]. To check whether these potential metabolites of 2-AG were involved in 2-AG-induced cell death, and to exclude that prostaglandin D2 (PGD2), the COX-2 metabolite of arachidonic acid, may also contribute to 2-AG-mediated cell death, primary HSCs were exposed to 100 μM of each substance.
Design and synthesis of novel prostaglandin E<inf>2</inf> ethanolamide and glycerol ester probes for the putative prostamide receptor(s)
2015, Tetrahedron LettersCitation Excerpt :Prostamides are a class of endogenous eicosanoids resulting from the cyclooxygenase-2 (COX-2) metabolism of the endocannabinoid anandamide (AEA).1,2
Metabolic Enzymes for Endocannabinoids and Endocannabinoid-Like Mediators
2015, The Endocannabinoidome: The World of Endocannabinoids and Related Mediators
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This work was supported by grants from the National Foundation for Cancer Research and the National Institutes of Health (CA89450 and GM15431).
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Correspondence to: Lawrence J. Marnett, Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232-0146, USA. Tel.: +615-343-7328; Fax: +615-343-7534; E-mail: [email protected]