Interactions of the Alkyl-Ether-Phospholipid, Platelet Activating Factor (PAF) with Platelets, Neural Cells, and the Psychotropic Drugs Triazolobenzodiazepines

Author(s):  
E. Kornecki ◽  
R. H. Lenox ◽  
D. H. Hardwick ◽  
J. A. Bergdahl ◽  
Y. H. Ehrlich
Endocrinology ◽  
1989 ◽  
Vol 125 (2) ◽  
pp. 1067-1073 ◽  
Author(s):  
RENATO BERNARDINI ◽  
ALDO E. CALOGERO ◽  
YIGAL H. EHRLICH ◽  
THOMAS BRUCKE ◽  
GEORGE P. CHROUSOS ◽  
...  

2019 ◽  
Vol 2019 (4) ◽  
Author(s):  
Rebecca Hills ◽  
Satoshi Ishii ◽  
Sonia Jancar ◽  
Thomas McIntyre ◽  
Ewa Ninio ◽  
...  

Platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is an ether phospholipid mediator associated with platelet coagulation, but also subserves inflammatory roles. The PAF receptor (provisional nomenclature recommended by NC-IUPHAR [37]) is activated by PAF and other suggested endogenous ligands are oxidized phosphatidylcholine [73] and lysophosphatidylcholine [96]. It may also be activated by bacterial lipopolysaccharide [89].


1990 ◽  
Author(s):  
Αντώνιος Ζάγκλης

The renal glomerulus and its various cell types (i.e. mesangial cells, endothelial cells) have been shown to synthesize compounds with autacoid and proinflammatory effects. [97,98] The spectrum of proinflammatory compounds of glomerular origin has recently expanded to include the alkyl ether glycerophospholipids, including 1-O-alkyl-2- acetyl-sn- glycero-3- phosphorylcholine, which is structurally identical with platelet activating factor (PAF).This compound can induce platelet and neutrophil aggregation and chemokinesis, vasodilation, increased vascular permeability and stimulation of eicosanoid production. We have demonstrated that PAF can be both synthesized and degraded in isolated glomeruli and in mesangial cells, [7,99] the latter being also capable of de novo synthesis of PAF precursors. Recent observations indicate that PAF receptor antagonism ameliorates glomerular inflammation in rabbit nephrotoxic serum nephritis, as well as the glomerular inflammatory injury induced by in situ formation of immune complexes in the rat kidney with experimental passive reverse Arthus reaction. [100,101] The present study was undertaken in order to assess the levels and cellular sources of glomerular PAF in glomeruli isolated from rats with: 1) Nephrotoxic serum nephritis, an infiltrative and complement dependent model of immune injury and 2) passive Heymann nephritis a non- infiltrative but complement dependent model. The role of complement, platelets and polymorphonuclear leucocytes was assessed. The observation that mesangial cells is the main source of PAF production in the rat glomerulus, prompted the assessment of the effect of various inflammatory mediators on the acetyl-transferase activity of the mesangial cells. […]


2007 ◽  
Vol 426 (1) ◽  
pp. 59-63 ◽  
Author(s):  
Anja Boetkjaer ◽  
Merete Boedker ◽  
Jian-Guo Cui ◽  
Yuhai Zhao ◽  
Walter J. Lukiw

1981 ◽  
Author(s):  
C M Chesney ◽  
D D Pifer ◽  
L M Cagen ◽  
E E Muirhead

Kishimoto et al.(J.B.C.255:2273,1980) have demonstrated a Ca2+ and phospholipid-dependent protein kinase (PK) from various mammalian tissues which is markedly stimulated by the addition of unsaturated diacylglycerol. PAF, an alkyl ether analogue of phosphatidyl choline induces platelet aggregation and secretion. We investigated the ability of the C18:0 analogue (l-alkyl-2acetyl-sn-glycero-3-phosphocholine) to stimulate Ca2+ dependent PK activity in homogenates of human platelets. Two hundred ml whole blood was collected in EDTA(5mM) and EGTA(5mM). PGl2(534nM) was included to prevent platelet activation during preparation. Platelets were washed twice in 0.05M Tris containing EDTA, EGTA,and PGl2, pH 7.5. On the 3rd wash PGI2 was omitted. The platelet pellet was then resuspended in the same buffer now containing leu- peptin(0.2mM) to inhibit proteolytic activation of PK. The suspension was sonicated and centrifuged at 100,000xg for 1 hr. PK activity was assayed in the supernatant and pellet suspension by measuring the incorporation of 32P into HI histone from [γ32P]ATP. The standard reaction mixture (0.3 ml) contained 250yl supernatant or pellet suspension, HI histone(60μg), [γ32P]ATP(3nmoles),magnesium acetate (13.3mM) diolein(500ng) Ca2+ and PAF for 3 min. at 30°.Basal PK activity was 14.6pmol/min/mg protein. PAF(0.8μg) which is just saturating dose for in vitro platelet aggregation, stimulate PK activity by 70% in the supernatant but was without effect on the pellet suspension. In the absence of Ca2+ and/or diolein there was no stimulation of PK by PAF. Phosphatidyl serine(PS)(5μg) also stimulated protein kinase by 100%.Stimulation of PK by both PAF and PS occurred at endogenous platelet Ca2+ concentrations (i.e. sufficient Ca2+ added to titrate EDTA and EGTA) and at higher Ca2+ concentration (by 0.2mM.)Supernatants from platelets prepared in the absence of PGI2 were not stimulated by PAF These data show that PAF activates a Ca2+ dependent protein kinase which may mediate its effects on human platelets.


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