Platelet-activating factor stimulates the phosphatidylinositol cycle. Appearance of phosphatidic acid is associated with the release of serotonin in horse platelets.
Abstract: The addition of platelet-activating factor to horse platelets prelabeled with (32P)orthophosphate induces the rapid formation of [32P]phosphatidic acid. This is subsequently followed by a considerable increase in the labeling of phosphatidylinositol. Activation of the formation of phosphatidic acid by platelet-activating factor is evident at a concentration of 1 nM, is maximal at 0.1 microM, and independent of the presence or absence of plasma in the medium. In horse platelets prelabeled with [14C]arachidonic acid, platelet-activating factor stimulates the rapid formation of [14C]phosphatidic acid, [14C]arachidonic acid, and [14C]arachidonate metabolites. Concomitantly, there is a loss of radioactivity from phosphatidylinostiol., phosphatidylcholine, and phosphatidylethanolamine. Platelet-activating factor at a concentration of 1 nM stimulates formation of phosphatidic acid while the appearance of arachidonate metabolites is seen at a higher concentration (10 nM), without acetate in the 2-position, is unable to induce in platelets the formation of phosphatidic acid, arachidonate metabolites, or the release of [3H]serotonin and, in addition, does not antagonize the action of platelet-activating factor. the release of [3H]serotonin and [14C]arachidonate from platelets stimulated with platelet-activating factor is not affected by indomethacin. Trifluoperazine (50-100 microM) inhibits the platelet-activating factor-stimulated liberation of arachidonic acid from phospholipids, without affecting the formation of phosphatidic acid and the release of serotonin. Prostacyclin, on the other hand, inhibits the platelet-activating factor-induced release of serotonin, arachidonate metabolites, and formation of phosphatidic acid. These data indicate a close relationship between the formation of phosphatidic acid and the release of serotonin in platelets stimulated with the platelet-activating factor.
Publication Date: 1982-07-10 PubMed ID: 7045103
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- Journal Article
Summary
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This study examines how platelet-activating factor prompts the formation of phosphatidic acid and release of serotonin in horse platelets, suggesting a close link between these processes.
Methodology and Findings
- The researchers added Platelet-Activating Factor (PAF) to horse platelets that had been “pre-labeled” with (32P)orthophosphate. This induced the rapid creation of [32P]phosphatidic acid and then, a noticeable increase in the labeling of phosphatidylinositol.
- Activation of phosphatidic acid formation through PAF was noticeable at a concentration of 1 nM achieving maximum potency at 0.1 microM, and appeared unaffected by the presence or absence of plasma in the medium.
- When horse platelets were pre-labeled with [14C]arachidonic acid, PAF stimulated the formation of [14C]phosphatidic acid, [14C]arachidonic acid, and [14C]arachidonate metabolites. This corresponded with a decrease in radioactivity from phosphatidylinostiol, phosphatidylcholine, and phosphatidylethanolamine.
Interpretation of Findings
- The appearance of arachidonate metabolites occurred at higher PAF concentration (10 nM).
- The researchers found that a version of PAF with an absence of acetate in the 2-position was unable to stimulate the formation of phosphatidic acid, arachidonate metabolites, or the release of [3H]serotonin in platelets, while not inhibiting the effects of PAF.
- Indomethacin had no significant effect on the release of [3H]serotonin and [14C]arachidonate from platelets stimulated with PAF.
- The drug Trifluoperazine (at 50-100 microM concentrations) was found to inhibit PAF-stimulated liberation of arachidonic acid from phospholipids, but did not affect the formation of phosphatidic acid nor the release of serotonin.
- Prostacyclin, on the other hand, was seen to inhibit the PAF-induced release of serotonin, arachidonate metabolites, and the formation of phosphatidic acid.
These findings suggest a close relationship between the formation of phosphatidic acid and the release of serotonin in the presence of platelet-activating factor. This understanding about how PAF operates might prove useful for the research in blood clotting, inflammation, and other response involving platelets.
Cite This Article
APA
Lapetina EG.
(1982).
Platelet-activating factor stimulates the phosphatidylinositol cycle. Appearance of phosphatidic acid is associated with the release of serotonin in horse platelets.
J Biol Chem, 257(13), 7314-7317.
Publication
Researcher Affiliations
MeSH Terms
- Animals
- Arachidonic Acids / pharmacology
- Blood Platelets / drug effects
- Blood Platelets / metabolism
- Epoprostenol / pharmacology
- Horses
- Kinetics
- Lysophosphatidylcholines / pharmacology
- Phosphatidic Acids / blood
- Phosphatidylinositols / blood
- Platelet Activating Factor
- Serotonin / blood
- Trifluoperazine / pharmacology
Citations
This article has been cited 18 times.- Yim NH, Lee JJ, Lee B, Li W, Ma JY. Antiplatelet Activity of Acylphloroglucinol Derivatives Isolated from Dryopteris crassirhizoma. Molecules 2019 Jun 13;24(12).
- Grassi G, Cappello N, Gheorghe MF, Salton L, Di Bisceglie C, Manieri C, Benedetto C. Exogenous platelet-activating factor improves the motility of human spermatozoa evaluated with C.A.S.A.: optimal concentration and incubation time. J Endocrinol Invest 2010 Nov;33(10):684-90.
- Roudebush WE, Purnell ET, Stoddart NR, Fleming SD. Embryonic platelet-activating factor: temporal expression of the ligand and receptor. J Assist Reprod Genet 2002 Feb;19(2):72-8.
- Wardle TD, Hall L, Turnberg LA. Platelet activating factor: release from colonic mucosa in patients with ulcerative colitis and its effect on colonic secretion. Gut 1996 Mar;38(3):355-61.
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