Disease relevance of Monoethanolamine oleic acid amide

• To specify the site of the action of TNF-alpha, the myocytes were incubated with pertussis toxin or N-oleoylethanolamine, a ceramidase inhibitor, and IK was measured [1].
• N-Oleoylethanolamine inhibits glucosylation of natural ceramides in CHP-100 neuroepithelioma cells: possible implications for apoptosis [2].
• Methods: Ceramide levels were modified using N-oleoylethanolamine (NOE), sphingosine-1-phosphate (S1P) as well as through serum deprivation, in LNCaP, DU145 and PC-3 prostate cancer cells [3].

High impact information on Monoethanolamine oleic acid amide

• N-oleoylethanolamine, which is known to inhibit ceramidase activity, unexpectedly downregulated acid ceramidase and accelerated radiation-induced apoptosis in U87-W E6 cells [4].
• Treating PCC7-Mz1 stem cells with a neutral sphingomyelinase or with the ceramidase inhibitor N-oleoylethanolamine elevated the endogenous ceramide levels and concomitantly induced apoptosis [5].
• Furthermore, in the presence of an acidic ceramidase inhibitor, N-oleoylethanolamine, TNFalpha leads to a sustained accumulation of ceramide and in parallel induces DNA fragmentation [6].
• Finally, blocking sphingosine production using an inhibitor of ceramidase, n-oleoylethanolamine, completely abrogated the negative inotropic effects of TNF-alpha in isolated contracting cardiac myocytes [7].
• An inhibitor of ceramidase activity, N-oleoylethanolamine, reduced PDGF- but not endothelin-1-stimulated proliferation [8].

Chemical compound and disease context of Monoethanolamine oleic acid amide

• Both pre-incubation with pertussis toxin and N-oleoylethanolamine abolished the inhibitory action of TNF-alpha on isoproterenol-augmented IK [1].

Biological context of Monoethanolamine oleic acid amide

• Previous work has demonstrated that down-regulation of ceramide production after selection of cells with N-oleoylethanolamine (OE), an inhibitor of ceramidase, results in resistance to DNA damage-induced apoptosis [9].
• N-oleoyl ethanolamine did not cause cell death by itself [10].
• It was found that unsaturated NAEs, N-oleoylethanolamine (N-Ole) and, to a greater extent, N-arachidonoylethanolamine (N-Ara), inhibited predominantly complex I of the respiratory chain, with a much weaker effect on complexes II and III, and no effect on complex IV [11].
• The lack of inhibition by several mammalian CDase inhibitors such as D-erythro-MAPP, L-erythro-MAPP or N-oleoylethanolamine points to a novel active site and/or substrate binding region [12].
• Fatty acid amide hydrolase (FAAH) is a membrane-associated enzyme that catalyzes the hydrolysis of several endogenous bioactive lipids, including anandamide (AEA), N-palmitoylethanolamine (PEA), oleamide, and N-oleoylethanolamine (OEA) [13].

Anatomical context of Monoethanolamine oleic acid amide

• N-Oleoylethanolamine activated PAL2 expression in leaves and diminished [(3)H]NAE 14:0 binding in microsomes, whereas N-linoleoylethanolamine did not activate PAL2 expression in leaves, and did not affect [(3)H]NAE 14:0 binding in microsomes [14].
• In addition, preincubation with N-oleoylethanolamine, a specific inhibitor of ceramidase, did not affect BK action on PLD in young fibroblasts but significantly decreased the effect of the peptide in old fibroblasts [15].
• However, in spite of making the matrix space accessible to external [14C]sucrose, N-arachidonoylethanolamine and N-oleoylethanolamine resulted in only a limited swelling of mitochondria and diminished the rate of swelling produced by high Ca2+ load [16].
• The discovery of endogenous fatty acyl amides such as N-arachidonoyl ethanolamide (anandamide), N-oleoyl ethanolamide (OEA), and N-arachidonoyl dopamine (NADA) as important signaling molecules in the central and peripheral nervous system has led us to pursue other unidentified signaling molecules [17].

Associations of Monoethanolamine oleic acid amide with other chemical compounds

• To assess the roles of the sphingomyelin and NO pathways in TNF-alpha and IL-1beta cross-signaling, the ceramidase inhibitor N-oleoyl ethanolamine (1 microM) or the NO synthase inhibitor N(G)-monomethyl-L-arginine (10 microM) was added before TNF-alpha (125 pg/mL) or IL-1beta (50 pg/mL) [18].

Gene context of Monoethanolamine oleic acid amide

• In contrast, the accumulations of two other N-acylethanolamines, N-oleoylethanolamine (OEA) and N-palmitoylethanolamine (PEA), were not reduced at 24 h postmortem in either the FAAH-/- mice or mice treated with URB532 [19].
• An inhibitor of the sphingolipid signaling pathway, N-oleoylethanolamine (NOE, 1 microm) attenuated ischemic and TNF alpha preconditioning [20].
• Neither N-oleoylethanolamine (OE, ceramidase inhibitor) or d,l-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP, an inhibitor of glucosylceramide synthase and the formation of 1-O-acyl ceramides) prevented the action of PAF [21].
• Using an N-oleoyl ethanolamide scaffold, a series of phosphate polar head group analogues of LPA comprised of various alpha-substituted phosphonates and thiophosphates was prepared [22].

Analytical, diagnostic and therapeutic context of Monoethanolamine oleic acid amide

• In contrast, NOE did not reverse ischemic preconditioning enhanced post-ischemic contractile function [20].

References