Enhancement of Thrombin-Induced Degradation of Phosphatidylcholine in Reserpinized Rabbit Platelets

1981 ◽  
Vol 46 (03) ◽  
pp. 655-657 ◽  
Author(s):  
Yasuko Watanabe ◽  
Masako Soda ◽  
Bonro Kobayashi
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Phosphatidyl Ethanolamine ◽  
Rabbit Platelets ◽  
Tlc Analysis ◽  
Oxygenated Products ◽  
Stimulation Of

SummaryWhen 1-14C-arachidonic acid-labeled, washed platelets from the reserpinized rabbits were exposed to thrombin, the decrease in radioactivity of phospholipids was significantly stimulated as compared with the control platelets. The increase in radioactivity of fatty acids and their oxygenated metabolites was also stimulated. TLC analysis revealed that the stimulation of the decrease in radioactivity of phospholipids was almost exclusively attributed to that of phosphatidylcholine (PC), and that thrombin induced a slight but significant increase in radioactivity of phosphatidyl ethanolamine (PE) in the reserpinized platelets. The results suggest that thrombin-induced degradation of PC is enhanced in the reserpinized platelets, and the overproduced fatty acids would be metabolized to the larger amount of oxygenated products which result in the activation of the platelets. Thrombin-induced mobilization of PC to PE in the reserpinized platelet phospholipids was also suggested.

scholarly journals Adrenaline Stimulation of Phospholipid Metabolism in Adipocyte Ghosts

1987 ◽  
Vol 40 (4) ◽  
pp. 405
Author(s):  
David Mann ◽  
Audrey M Bersten
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Linoleic Acid ◽  
Adenylate Cyclase ◽  
Phospholipid Metabolism ◽  
Dependent Manner ◽  
Long Chain Fatty Acids ◽  
Membrane Phospholipids ◽  
Dose Dependent ◽  
Stimulation Of

The incorporation of long-chain fatty acids into phospholipids has been detected in adipocyte ghosts that were incubated with [1_14 C] stearic, [1_14 C] linoleic or [l_14C] arachidonic acid. Adrenaline and adenosine activated this incorporation within 15 s of exposure of the ghosts to the hormones and the response was dose dependent. Maximum incorporation of labelled linoleic acid occurred at 10-5 M adrenaline and 10-7 M adenosine. The a-agonist phenylephrine and the ~-agonist isoproterenol were also shown to stimulate the incorporation of fatty acid in a dose dependent manner. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol were each labelled preferentially with linoleic or arachidonic acid. p-Bromophenacylbromide, quinacrine and centrophenoxine inhibited the adrenaline-stimulated incorporation of fatty acids into ghost membrane phospholipids, and p-bromophenacylbromide also reduced the activation of adenylate cyclase by adrenaline. NaF, an activator of adenylate cyclase, like adrenaline, stimulated the incorporation of linoleic acid into ghost membrane phospholipids.

scholarly journals Evidence from studies employing radioactively labelled fatty acids that the stimulation of flux through the diacylglycerol pool is an early action of vasopressin on hepatocytes

1987 ◽  
Vol 245 (1) ◽  
pp. 211-216 ◽  
Author(s):  
L B Pickford ◽  
A J Polverino ◽  
G J Barritt
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Phosphatidic Acid ◽  
Isolated Hepatocytes ◽  
Maximal Increase ◽  
Maximal Stimulation ◽  
Early Action ◽  
Palmitic Acids ◽  
Stimulation Of ◽  
In Cells

1. In isolated hepatocytes prelabelled with [14C]-arachidonic, -stearic, -linoleic, -oleic or -palmitic acids, vasopressin increased the amount of radioactivity present in diacylglycerols. The largest increase was observed in cells labelled with arachidonic or stearic acids. 2. In cells prelabelled with [14C]- or [3H]-arachidonic acid, the onset of the increase in radioactivity in diacylglycerols induced by vasopressin was slow, the increase was partly dependent on the presence of extracellular Ca2+, and was associated with an increase in radioactivity present in phosphatidic acid which was more rapid in onset. Vasopressin decreased the amount of [3H]arachidonyl-phosphatidylinositol 4,5-bisphosphate, but the magnitude of this decrease was less than 10% of the observed increase in radioactivity in [3H]arachidonyl-diacylglycerol. 3. The concentration of vasopressin which gave half-maximal increase in [14C]arachidonyl-diacylglycerol at low extracellular Ca2+ was 10-fold higher than that which gave half-maximal stimulation of 45Ca2+ efflux. Phenylephrine, but not glucagon, also increased the amount of [14C]arachidonyl-diacylglycerol. 4. It is concluded that an early action of vasopressin on the liver cell is to increase the flux of carbon from phospholipids, including the phosphoinositides, to diacylglycerols.

FATTY ACID COMPOSITION OF PHOSPHATIDYL ETHANOL-AMINE AND PHOSPHATIDYL SERINE FROM DOG BILE

1964 ◽  
Vol 42 (3) ◽  
pp. 309-316 ◽  
Author(s):  
U. K. Misra ◽  
D. A. Turner
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Stearic Acid ◽  
Palmitic Acid ◽  
Linolenic Acid ◽  
Phosphatidyl Ethanolamine ◽  
Phosphatidyl Serine ◽  
Fatty Acid Analysis

Phosphatidyl ethanolamine and phosphatidyl serine extracted from dog bile have been separated by means of ammonium silicate column chromatography. Concentration of phosphatidyl serine in dog bile is about seven times higher than phosphatidyl ethanolamine. Fatty acid analysis by gas chromatography showed that phosphatidyl ethanolamine contains about 26% palmitic acid, 18% stearic acid, 11% linoleic acid, 2% linolenic acid, 9% arachidonic acid, 3% C22:5 fatty acid, and 6% C22:6 fatty acid. The concentrations of these fatty acids observed in phosphatidyl serine are different; palmitic acid represents about 43%, stearic acid 9%, linoleic acid 24%, linolenic acid a trace amount, and arachidonic acid 5%; C22:5 and C22:6 fatty acids are absent.

scholarly journals Stimulation of anterior pituitary prostaglandin E content and somatotropin (growth hormone) synthesis by phospholipase A

1978 ◽  
Vol 176 (1) ◽  
pp. 319-323 ◽  
Author(s):  
A Betteridge ◽  
M Wallis
Keyword(s):  
Fatty Acids ◽  
Growth Hormone ◽  
Arachidonic Acid ◽  
Anterior Pituitary ◽  
Phospholipase A ◽  
Prostaglandin E ◽  
Specific Response ◽  
Hormone Synthesis ◽  
Pituitary Glands ◽  
Stimulation Of

The prostaglandin E content of dispersed rat anterior pituitary glands was found to increase in the presence of phospholipase A or arachidonic acid. The increases were abolished by the addition of indomethacin. Similarly, the rate of somatotropin (growth hormone) synthesis was increased by these two agents, and the increases were again abolished by indomethacin. Phospholipase A also stimulated somatotropin release. The stimulation of prostaglandin E accumulation was a specific response to those fatty acids that are precursors for prostaglandin synthesis. One such precursor, [3H]arachidonic acid, was incorporated by rat anterior pituitary glands in vitro, and found to be associated mainly with phosphatidylethanolamine-like material. It is concluded that the intracellular concentration of prostaglandin E is limited by the availability of precursor fatty acids and that this can be increased by the addition of exogenous precursors or by the action of exogenous phospholipase A on the cellular phospholipid. Factors that increased prostaglandin E concentrations also increase the rate of synthesis of somatotropin, providing further evidence for the concept that prostaglandin E is involved in modulation of the rate of synthesis of this hormone.

scholarly journals Influence of arachidonic acid on indices of phospholipase A2 activity in the human neutrophil

1993 ◽  
Vol 291 (3) ◽  
pp. 825-831 ◽  
Author(s):  
J D Winkler ◽  
C M Sung ◽  
W C Hubbard ◽  
F H Chilton
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Protein Kinase ◽  
Phospholipase A2 ◽  
Human Neutrophils ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Pla2 Activity ◽  
Tetraenoic Acid ◽  
Stimulation Of

The present studies were conducted to understand better the regulation of phospholipase A2 (PLA2)-dependent mobilization of lipid mediators by arachidonic acid (C20:4). After stimulation of human neutrophils, g.l.c./m.s. analysis of non-esterified fatty acids indicated that the quantity of C20:4 increased as a function of time after stimulation, from undetectable quantities to > 800 pmol/10(7) cells. In contrast with C20:4, the quantities of other free fatty acids such as oleic and linoleic were high in resting cells and did not change after stimulation. Some 15% of the C20:4 released from cellular lipids remained cell-associated. To examine the effect of C20:4 on its own release, neutrophils were exposed to [2H8]C20:4, to differentiate it by g.l.c./m.s. from naturally occurring C20:4. In A23187-stimulated neutrophils, low concentrations (5-10 microM) of [2H8]C20:4 added just before A23187 increased the quantity of C20:4 produced by the cell, whereas higher concentrations (30-50 microM) decreased the quantity of C20:4 released from phospholipids. As other measures of PLA2 activity, the effects of C20:4 on production of platelet-activity factor (PAF) and leukotriene B4 (LTB4) were assessed. C20:4 treatment just before stimulation of neutrophils blocked PAF and LTB4 production in a concentration-dependent manner (IC50 10-20 microM). The effect of C20:4 was not blocked by the cyclo-oxygenase inhibitor naproxine (10 microM), nor could it be mimicked by 1 microM LTB4, 5-hydroxyeicosa-6,8,11,14-tetraenoic acid (5HETE), 5-hydroperoxyeicosa-6,8,11,14-tetraenoic acid (5HPETE) or 15-hydroxyeicosa-5,8,11,13-tetraenoic acid (15HETE). The 5-lipoxygenase (5LO) inhibitor zileuton induced a concentration-dependent decrease in PAF, with a maximal effect of a 50% decrease at 10-50 microM. The decrease in PAF by the 5LO inhibitor could not be circumvented by addition of 1 microM 5HETE, 5HPETE and LTB4, and may be attributed to the capacity of zileuton to increase the quantity of C20:4 in A23187-treated neutrophils. The inhibitory effect of C20:4 (20-40 microM) on PAF production could be antagonized by the protein kinase C inhibitor staurosporine (30 nM), but not by inhibitors of protein kinase A, tyrosine kinase or calmodulin kinase II. Taken together, these data demonstrate that C20:4 is selectively released from membrane phospholipids of A23187-stimulated neutrophils, and this C20:4 may play an important role in regulating the mobilization of C20:4 by altering PLA2 activity.

scholarly journals Thrombin-Induced Changes in Phosphatidic ACID (PA) and Phosphoinositides

1977 ◽  
Author(s):  
N. L. Leung ◽  
R. L. Kinlough-Rathbone ◽  
J. F. Mustard
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Thin Layer ◽  
Phospholipid Metabolism ◽  
Rabbit Platelets ◽  
Inositol Phospholipid ◽  
Induced Changes ◽  
Layer Chromatography ◽  
Stimulation Of

Thrombin-induced changes in PA, monophosphoinositide (MPI) , diphosphoinositide (DPI) and triphosphoinositide (TPI) of washed rabbit platelets have been examined. Platelets prelabeled by incubation with 32P-orthophosphate, 3H-glycerol, 3H-inositol or 14C-arachidonate were exposed to 0.33 u/ml thrombin for one minute, and the phospholipids extracted and separated by thin layer chromatography. Measurement of absolute amounts of PA and MPI by phosphorus assay showed that PA increased by 180% while MPI decreased by 15%.The changes in MPI with 3H-G, 3H-I and 14C-AA and in 1,2-diacyl glycerol (DG) indicate that some MPI may be converted to PA via DG. Changes in the 3H-G and 3H-I labeling of DPI and TPI suggest that the changes observed with 32P-Iabeled platelets are a result of the turnover of the phosphorylinositol moiety. The increase in AA with 14C-AA indicates that some of the decrease in MPI may be due to the formation of lyso MPI and free fatty acid. These results indicate that thrombin stimulation of platelets may affect inositol phospholipid metabolism through three pathways: (1) involving PA, DG and MPI; (2) the cleavage of free fatty acids from MPI; (3) turnover of the ester phosphates on DPI and TPI.

scholarly journals Effects of fatty acids and fatty acyl CoA esters on arachidonic acid (AA) metabolism in rabbit platelets.

1994 ◽  
Vol 64 ◽  
pp. 194
Author(s):  
Yohko Fujimoto ◽  
Masahide Tsunomori ◽  
Hiroko Nishida ◽  
Satoru Sakuma ◽  
Tadashi Fujita
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Fatty Acyl ◽  
Rabbit Platelets

Eicosapentaenoic Acid Interferes with U46619-Stimulated Formation of Inositol Phosphates in Washed Rabbit Platelets

1989 ◽  
Vol 62 (04) ◽  
pp. 1116-1120 ◽  
Author(s):  
N Chetty ◽  
J D Vickers ◽  
R L Kinlough-Rathbone ◽  
M A Packham ◽  
J F Mustard
Keyword(s):  
Signal Transduction ◽  
Fatty Acid Composition ◽  
Eicosapentaenoic Acid ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Dense Granule ◽  
Detectable Change ◽  
Membrane Phospholipids ◽  
Rabbit Platelets ◽  
Stimulation Of

SummaryEicosapentaenoic acid (EPA) inhibits platelet responsiveness to aggregating agents. To investigate the reactions that are affected by EPA, we examined the effect of preincubating aspirintreated rabbit platelets with EPA on stimulation of inositol phosphate formation in response to the TXA2 analogue U46619. Stimulation of platelets with U46619 (0.5 μM) caused aggregation and slight release of dense granule contents; aggregation and release were inhibited by preincubation of the platelets with EPA (50 μM) for 1 h followed by washing to remove unincorporated EPA. Incubation with EPA (50 μM) for 1 h did not cause a detectable increase in the amount of EPA in the platelet phospholipids. When platelets were prelabelled with [3H]inositol stimulation with U46619 of control platelets that had not been incubated with EPA significantly increased the labelling of mos1tol phosphates. The increases in inositol phosphate labelling due to U46619 at 10 and 60 s were partially inhibited by premcubat10n of the platelets with 50 μM EPA. Since the activity of cyclo-oxygenase was blocked with aspirin, inhibition of inositol phosphate labelling in response to U46619 indicates either that there may be inhibition of signal transduction without a detectable change in the amount of EPA in platelet phospholipids, that changes in signal transduction require only minute changes in the fatty acid composition of membrane phospholipids, or that after a 1 h incubation with EPA, activation of phospholipase C is affected by a mechanism that is not directly related to incorporation of EPA.

Inhibition by Glaucocalyxin A of Aggregation of Rabbit Platelets Induced by ADP, Arachidonic Acid and Platelet-Activating Factor, and Inhibition of [3H]-PAF Binding

1992 ◽  
Vol 67 (04) ◽  
pp. 458-460 ◽  
Author(s):  
Zhang Bin ◽  
Long Kun
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Activating Factor ◽  
Northeastern China ◽  
Ethereal Extract ◽  
Ic50 Value ◽  
Rabbit Platelets ◽  
Ic50 Values ◽  
Induced Aggregation

SummaryGlaucocalyxin A is a new diterpenoid isolated from the ethereal extract of the leaves of Rabdosia japonica (Burm f) Hara var glaucocalyx (Maxim) Hara (Labiatae) collected in the northeastern China. When it was incubated with washed rabbit platelets, glaucocalyxin A inhibited ADP- or arachidonic acid-induced platelet aggregation with IC50 values of 4.4 μmol/1, 14.1 μmol/1 respectively. Glaucocalyxin A also inhibited PAF-induced aggregation of rabbit platelets which were refractory to ADP and arachidonic acid with an IC50 value of 13.7 μmol/1. Analysis of [3H]-PAF binding showed that glaucocalyxin A prevented [3H]-PAF binding to intact washed rabbit platelets with an IC50 value of 8.16 μmol/1, which was consistent with its inhibition of PAF-induced platelet aggregation.

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