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Journal articles on the topic 'Platelet activating factor. Arachidonic acid'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Holub, Bruce J., Diana J. Philbrick, Anwar Parbtani, and William F. Clark. "Dietary lipid modification of renal disorders and ether phospholipid metabolism." Biochemistry and Cell Biology 69, no. 7 (1991): 485–89. http://dx.doi.org/10.1139/o91-072.

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The formation of arachidonic acid derived eicosanoids, including thromboxane A2 and leukotriene B4, as well as platelet-activating factor (1-O-alkyl-2-acetyl-glycerophosphocholine), has been implicated in various renal pathophysiologies. Alteration of the fatty acid composition of membrane phospholipids in platelets, the glomerulus, and inflammatory cells, and of 1-O-alkyl-2-acyl-glycerophosphocholine (platelet-activating factor precursor) can be attained by dietary lipid modifications (e.g., consumption of fish oil containing n – 3 polyunsaturated fatty acids). These changes have been associa

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IZAKI, S., T. YAMAMOTO, Y. GOTO, et al. "Platelet-activating factor and arachidonic acid metabolites in psoriatic inflammation." British Journal of Dermatology 134, no. 6 (1996): 1060–64. http://dx.doi.org/10.1111/j.1365-2133.1996.tb07943.x.

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IZAKI, S., T. YAMAMOTO, Y. GOTO, et al. "Platelet-activating factor and arachidonic acid metabolites in psoriatic inflammation." British Journal of Dermatology 134, no. 6 (1996): 1060–64. http://dx.doi.org/10.1046/j.1365-2133.1996.d01-902.x.

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4

Nakajima, Toshiaki, Tsuneaki Sugimoto, and Yoshihisa Kurachi. "Platelet-activating factor activates cardiac GK via arachidonic acid metabolites." FEBS Letters 289, no. 2 (1991): 239–43. http://dx.doi.org/10.1016/0014-5793(91)81079-n.

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5

Bin, Zhang, and Long Kun. "Inhibition by Glaucocalyxin A of Aggregation of Rabbit Platelets Induced by ADP, Arachidonic Acid and Platelet-Activating Factor, and Inhibition of [3H]-PAF Binding." Thrombosis and Haemostasis 67, no. 04 (1992): 458–60. http://dx.doi.org/10.1055/s-0038-1648470.

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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 glau

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Ahmed, Y., M. H. F. Sullivan, and M. G. Elder. "Detection of Platelet Desensitization in Pregnancy-Induced Hypertension Is Dependent on the Agonist Used." Thrombosis and Haemostasis 65, no. 05 (1991): 474–77. http://dx.doi.org/10.1055/s-0038-1648174.

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SummaryThe aggregation of platelets from women with pregnancy-induced hypertension (P.I.H.), or with normal pregnancies, in response to arachidonic acid, ADP, collagen or platelet activating factor (PAF) was examined. No differences in platelet aggregation between the normotensive and hypertensive women were detected when arachidonic acid or collagen were used to stimulate in vitro platelet aggregation. Higher concentrations of ADP and PAF were required to aggregate platelets from women with P.I.H. compared with platelets from normotensive controls. Platelets from women with normotensive pregn

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7

Saeed, S. A., R. U. Simjee, G. Shamim, and A. H. Gilani. "Eugenol: a dual inhibitor of platelet-activating factor and arachidonic acid metabolism." Phytomedicine 2, no. 1 (1995): 23–28. http://dx.doi.org/10.1016/s0944-7113(11)80044-9.

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8

Ramesha, C. S., and W. C. Pickett. "Metabolism of platelet-activating factor by arachidonic acid-depleted rat polymorphonuclear leukocytes." Journal of Biological Chemistry 261, no. 33 (1986): 15519–23. http://dx.doi.org/10.1016/s0021-9258(18)66744-4.

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9

Livio, M., G. Vigano, M. Morigi, A. Ubiali, M. Galbusera, and G. Remuzzi. "Role of platelet-activating factor in primary hemostasis." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 6 (1988): H1218—H1223. http://dx.doi.org/10.1152/ajpheart.1988.254.6.h1218.

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To determine whether platelet-activating factor (PAF) has a physiological role in the process of primary hemostasis in the rabbit, we measured skin bleeding times in animals given orally a specific PAF-receptor antagonist L-652,731. One hour after the administration of L-652,731 (20 or 40 mg/kg), a significant prolongation of bleeding time was observed. Parameters known to interfere with the process of primary hemostasis were not altered by PAF-receptor antagonist. In addition, no changes were observed in platelet count and vessel wall arachidonic acid metabolism, as revealed by serum thrombox

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10

Garcia, M. D. C., S. Fernandez-Gallardo, M. A. Gijon, C. Garcia, M. L. Nieto, and M. Sanchez Crespo. "Biosynthesis of platelet-activating factor (PAF) in human polymorphonuclear leucocytes. The role of lyso-PAF disposal and free arachidonic acid." Biochemical Journal 268, no. 1 (1990): 91–98. http://dx.doi.org/10.1042/bj2680091.

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Theophylline and 1-methyl-3-isobutylxanthine (MIX), compounds that block eicosanoid formation and modulate phospholipase A2 activity, inhibited in a dose-dependent manner the formation of both leukotriene B4 (LTB4) and platelet-activating factor (PAF) by human polymorphonuclear leucocytes (PMN) in response to ionophore A23187. Theophylline and MIX lacked any inhibitory effect on acetyl-CoA: lyso-PAF acetyltransferase activity, which is the rate-limiting step for PAF biosynthesis in PMN. The effect of theophylline and MIX on PAF formation could be reversed by incubating the cells in the presenc

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11

Underwood, D. C., and P. J. Kadowitz. "Analysis of bronchoconstrictor responses to platelet-activating factor in the cat." Journal of Applied Physiology 67, no. 1 (1989): 377–82. http://dx.doi.org/10.1152/jappl.1989.67.1.377.

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Bronchoconstrictor responses to platelet-activating factor (PAF) were investigated in paralyzed, anesthetized, mechanically ventilated cats. Intravenous injections of PAF caused dose-dependent increases in lung resistance (RL) and decreases in dynamic compliance (Cdyn) and systemic arterial (aortic) pressure (PAO). The increases in RL and decreases in Cdyn in response to PAF were markedly reduced by sodium meclofenamate, a cyclooxygenase inhibitor, whereas the decreases in PAO were unchanged. Increases in RL and decreases in Cdyn but not PAO in response to PAF were reduced by SQ 29,548, a thro

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12

Heinroth-Hoffmann, I., A. Hauser, and H. J. Mest. "Effects of platelet activating factor antagonists on arachidonic acid-induced platelet aggregation and TXA2 formation." Prostaglandins, Leukotrienes and Essential Fatty Acids 41, no. 3 (1990): 181–82. http://dx.doi.org/10.1016/0952-3278(90)90087-2.

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13

Schlondorff, D., and R. Neuwirth. "Platelet-activating factor and the kidney." American Journal of Physiology-Renal Physiology 251, no. 1 (1986): F1—F11. http://dx.doi.org/10.1152/ajprenal.1986.251.1.f1.

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Platelet-activating factor (PAF) represents a group of phospholipids with the basic structure of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine. A number of different cells are capable of producing PAF in response to various stimuli. The initial step of PAF formation is activation of phospholipase A2 in a calcium-dependent manner, yielding lyso-PAF. During this step arachidonic acid is also released and can be converted to its respective cyclooxygenase and lipoxygenase products. The lyso-PAF generated is then acetylated in position 2 of the glycerol backbone by a coenzyme A (CoA)-dependent acety

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14

Pignatelli, Pasquale, Luciano De Biase, Luisa Lenti та ін. "Tumor necrosis factor-α as trigger of platelet activation in patients with heart failure". Blood 106, № 6 (2005): 1992–94. http://dx.doi.org/10.1182/blood-2005-03-1247.

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Abstract The clinical history of patients with heart failure (HF) is complicated by arterial thromboembolism. Platelet activation is reported in this population, but the underlying mechanism has not been clarified. Forty-two patients with HF scored according to New York Heart Association (NYHA) classification had higher levels of collagen-induced platelet aggregation, platelet tumor necrosis factor-α (TNF-α) receptor expression, and serum thromboxane B2 and higher circulating levels of TNF-α than 20 healthy subjects. Coincubation of platelets from HF patients with an inhibitor of TNF-α recepto

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15

Jørgensen, Katarina Mariann, Hanne Solvang Felberg, Rolf K. Berge, Astrid Lægreid, and Berit Johansen. "Platelet activating factor stimulates arachidonic acid release in differentiated keratinocytes via arachidonyl non-selective phospholipase A2." Archives of Dermatological Research 302, no. 3 (2009): 221–27. http://dx.doi.org/10.1007/s00403-009-1017-8.

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16

Tessner, T. G., J. T. O'Flaherty, and R. L. Wykle. "Stimulation of Platelet-activating Factor Synthesis by a Nonmetabolizable Bioactive Analog of Platelet-activating Factor and Influence of Arachidonic Acid Metabolites." Journal of Biological Chemistry 264, no. 9 (1989): 4794–99. http://dx.doi.org/10.1016/s0021-9258(18)83660-2.

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17

Naraba, Hiroaki, Akinori Ueno, and Sachiko Oh-ishi. "Effect of arachidonic acid on platelet-activating factor biosynthesis in rat polymorphonuclear leukocytes." Japanese Journal of Pharmacology 64 (1994): 194. http://dx.doi.org/10.1016/s0021-5198(19)50410-3.

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18

SAEED, SHEIKH A., NAZLI ALI, and SAIRA SALEEM. "Differential Effects of Anti-Asthmatic Drugs on Arachidonic Acid and Platelet-Activating Factor." Biochemical Society Transactions 22, no. 4 (1994): 443S. http://dx.doi.org/10.1042/bst022443s.

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19

Naraba, Hiroaki, Akinori Ueno, Hideki Matsumoto, and Sachiko Oh-ishi. "Inhibitory effect of arachidonic acid on platelet-activating factor production in rat neutrophils." European Journal of Pharmacology 302, no. 1-3 (1996): 117–21. http://dx.doi.org/10.1016/0014-2999(96)00029-5.

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20

Hideaki, Kawaguchi, and Yasuda Hisakazu. "Effect of platelet-activating factor on arachidonic acid metabolism in renal epithelial cells." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 875, no. 3 (1986): 525–34. http://dx.doi.org/10.1016/0005-2760(86)90073-1.

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21

Ammit, Alaina Jean, and Chris O'Neill. "Platelet-activating factor (PAF) receptor antagonists inhibit arachidonic acid induced platelet aggregation in rabbit whole blood." Lipids 26, no. 12 (1991): 1189–92. http://dx.doi.org/10.1007/bf02536529.

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22

Barr, RM, F. Lawlor, MR Judge, et al. "Platelet activating factor, lyso-platelet activating factor and arachidonic acid release in normal human skin and the influence of topical steroid treatment." British Journal of Clinical Pharmacology 35, no. 6 (1993): 637–41. http://dx.doi.org/10.1111/j.1365-2125.1993.tb04194.x.

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23

Kermode, John C., Qi Zheng, and Elizabeth P. Milner. "Marked Temperature Dependence of the Platelet Calcium Signal Induced by Human von Willebrand Factor." Blood 94, no. 1 (1999): 199–207. http://dx.doi.org/10.1182/blood.v94.1.199.413k14_199_207.

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Interaction of von Willebrand factor (vWF) with the platelet is essential to hemostasis when vascular injury occurs. This interaction elevates the intracellular free calcium concentration ([Ca2+]i) and promotes platelet activation. The present study investigated the temperature dependence of vWF-induced [Ca2+]i signaling in human platelets. The influence of temperature can provide invaluable insight into the underlying mechanism. Platelet [Ca2+]i was monitored with Fura-PE3. Ristocetin-mediated binding of vWF induced a transient platelet [Ca2+]i increase at 37°C, but no response at lower tempe

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24

Dusting, GJ, and AG Stewart. "Overview of eicosanoid metabolism and relationship to platelet-activating factor." Reproduction, Fertility and Development 2, no. 5 (1990): 417. http://dx.doi.org/10.1071/rd9900417.

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The pathways of arachidonic acid metabolism are becoming increasingly complex. Although it is unlikely that every pharmacological action of these eicosanoids reflects a physiological function, some of these compounds undoubtedly act as mediators of pathophysiological processes. Analogues of PGs have been exploited to a limited extent, and the emphasis for future therapeutic approaches will be on development of specific inhibitors and antagonists of eicosanoids that will alter the profile of products formed. These will be in the areas of inflammation (including asthma), cytoprotection of gastri

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25

Burka, J. F. "The interaction of histamine with other bronchoconstrictor mediators." Canadian Journal of Physiology and Pharmacology 65, no. 3 (1987): 442–47. http://dx.doi.org/10.1139/y87-075.

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The lack of therapeutic efficacy of antihistaminic drugs in the treatment of asthma has led to the search and discovery of other bronchoconstrictor agents, particularly leukotrienes, thromboxanes, and platelet-activating factor. However, specific receptor antagonist for any of these substances have also not been particularly effective in inhibiting allergic bronchoconstriction. It is now generally accepted that histamine, arachidonic acid metabolites, platelet-activating factor, and possibly other substances are all involved to varying degrees in asthma and may indeed interact. This paper revi

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26

Bioque, G., D. Tost, D. Closa, et al. "Concurrent C18 Solid Phase Extraction of Platelet Activating Factor (PAF) and Arachidonic Acid Metabolites." Journal of Liquid Chromatography 15, no. 8 (1992): 1249–58. http://dx.doi.org/10.1080/10826079208018285.

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27

Saeed, Sheikh, Rukhsana Simjee, Farah Mahmood, and Naheed Sultana. "Rhazimine fromRhazya stricta: A Dual Inhibitor of Arachidonic Acid Metabolism and Platelet Activating Factor-Induced Platelet Aggregation." Planta Medica 59, no. 06 (1993): 566–67. http://dx.doi.org/10.1055/s-2006-959765.

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28

Oestvang, Janne, Marit W. Anthonsen, and Berit Johansen. "LysoPC and PAF Trigger Arachidonic Acid Release by Divergent Signaling Mechanisms in Monocytes." Journal of Lipids 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/532145.

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Oxidized low-density lipoproteins (LDLs) play an important role during the development of atherosclerosis characterized by intimal inflammation and macrophage accumulation. A key component of LDL is lysophosphatidylcholine (lysoPC). LysoPC is a strong proinflammatory mediator, and its mechanism is uncertain, but it has been suggested to be mediated via the platelet activating factor (PAF) receptor. Here, we report that PAF triggers a pertussis toxin- (PTX-) sensitive intracellular signaling pathway leading to sequential activation of sPLA2, PLD, cPLA2, and AA release in human-derived monocytes

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Tao, W., T. F. P. Molski, and R. I. Sha'afi. "Arachidonic acid release in rabbit neutrophils." Biochemical Journal 257, no. 3 (1989): 633–37. http://dx.doi.org/10.1042/bj2570633.

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[3H]Arachidonic acid is released after stimulation of rabbit neutrophils with fMet-Leu-Phe or platelet-activating factor (PAF). The release is rapid and dose-dependent, and is inhibited in phorbol 12-myristate 13-acetate (PMA)-treated rabbit neutrophils. The protein kinase C (PKC) inhibitor 1-(5-isoquinoline-sulphonyl)-2-methylpiperazine (H-7) prevents this inhibition. In addition, PMA increases arachidonic acid release in H-7-treated cells stimulated with fMet-Leu-Phe. [3H]Arachidonic acid release, but not the rise in the concentration of intracellular Ca2+, is inhibited in pertussis-toxin-tr

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Cox, Dermot, Yukio Motoyama, Jiro Seki, Toshiaki Aoki, Miwako Dohi, and Keizo Yoshida. "Pentamidine: A Non-Peptide GPIIb/IIIa Antagonist – In Vitro Studies on Platelets from Humans and Other Species." Thrombosis and Haemostasis 68, no. 06 (1992): 731–36. http://dx.doi.org/10.1055/s-0038-1646352.

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SummaryIn this paper we show that the non-peptide anti-parasite agent pentamidine is a broad spectrum anti-platelet agent with an IC50 of 1.1 µM in ADP-induced platelet aggregation in human platelet rich plasma (PRP). It had similar activity when collagen, arachidonic acid, platelet activating factor, thrombin and epinephrine were used. It had no effect on platelet intracellular cAMP levels. It inhibited 125I-fibrinogen, 125I-fibronectin and 125I-von Willebrand factor binding to ADP-activated fixed platelets with IC50 values of 160, 160 and 60 nM respectively. Pentamidine showed a high degree

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31

Jancar, Sonia, Patrick Thériault, Brigitte Provençal, Solange Cloutier, and Pierre Sirois. "Mechanism of action of platelet-activating factor on guinea-pig lung parenchyma strips." Canadian Journal of Physiology and Pharmacology 66, no. 9 (1988): 1187–91. http://dx.doi.org/10.1139/y88-195.

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The contribution of thromboxane A2 to platelet-activating factor (PAF)induced contraction of guinea-pig lung parenchyma strips (GPLPS) was investigated using an experimental design that allowed us to record the contractions of the tissues in parallel with the determination of thromboxane B2 (TXB2) levels in the organ baths by enzyme immunoassay. It was found that the first injection of PAF induced the contraction of GPLPS and the release of TXB2. Following subsequent additions of PAF to the same tissue, the contractile response was abolished but TXB2 levels were not significantly reduced. Pret

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32

Handa, R. K., J. W. Strandhoy, and V. M. Buckalew. "Platelet-activating factor is a renal vasodilator in the anesthetized rat." American Journal of Physiology-Renal Physiology 258, no. 6 (1990): F1504—F1509. http://dx.doi.org/10.1152/ajprenal.1990.258.6.f1504.

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In view of the potent vasoactive properties of platelet-activating factor (PAF), we investigated the renal hemodynamic effects of this lipid. C16-PAF (0.5-10 ng/kg) given as a bolus into the renal arterial circulation of pentobarbital sodium-anesthetized male Wistar rats produced a dose-dependent increase in renal blood flow (6-15%), before causing systemic hypotension. The PAF-induced renal vasodilation and systemic hypotension was independent of renal innervation, unaltered by eicosanoid synthesis inhibition with indomethacin or dexamethasone, unchanged by the nonselective dopamine-receptor

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33

Spiel, Alexander, Johann Bartko, Michael Schwameis, et al. "Increased platelet aggregation and in vivo platelet activation after granulocyte colony-stimulating factor administration." Thrombosis and Haemostasis 105, no. 04 (2011): 655–62. http://dx.doi.org/10.1160/th10-08-0530.

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SummaryGranulocyte colony-stimulating factor (G-CSF) stimulates the bone marrow to produce granulocytes and stem cells and is widely used to accelerate neutrophil recovery after chemotherapy. Interestingly, specific G-CSF receptors have been demonstrated not only on myeloid cells, but also on platelets. Data on the effects of G-CSF on platelet function are limited and partly conflicting. The objective of this study was to determine the effect of G-CSF on platelet aggregation and in vivo platelet activation. Seventy-eight, healthy volunteers were enrolled into this randomised, placebo-controlle

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Castellani, M. L., M. Felaco, F. Pandolfi, et al. "Mast Cells and Arachidonic Acid Cascade in Inflammation." European Journal of Inflammation 7, no. 3 (2009): 131–37. http://dx.doi.org/10.1177/1721727x0900700302.

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Prostaglandin D2 PGD2 is a major cyclooxygenase metabolite of arachidonic acid produced by mast cells and it is released following allergen challenge in diseases, such as allergic diseases. PGD2 may act as a neuromodulator and as an allergic and inflammatory mediator. In allergic diseases, activated mast cell synthesizes prostaglandin D2 (first cyclo-oxygenate mediator) which has bronchoconstrictive and vasodilating effects and attracts several leukocytes. It has been found that activated mast cells, challenged with physiological and non- physiological secretagogues, release elevated histamine

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Ramesha, C. S., and W. C. Pickett. "Platelet-activating factor and leukotriene biosynthesis is inhibited in polymorphonuclear leukocytes depleted of arachidonic acid." Journal of Biological Chemistry 261, no. 17 (1986): 7592–95. http://dx.doi.org/10.1016/s0021-9258(19)57436-1.

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Evans, T. W., K. F. Chung, D. F. Rogers, and P. J. Barnes. "Effect of platelet-activating factor on airway vascular permeability: possible mechanisms." Journal of Applied Physiology 63, no. 2 (1987): 479–84. http://dx.doi.org/10.1152/jappl.1987.63.2.479.

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We studied the effects of the potent inflammatory mediator, platelet-activating factor (PAF), on vascular permeability in airways (and other tissues) of guinea pigs by measuring extravasation of circulating Evans blue dye. PAF caused a dose-dependent increase in vascular permeability. At 1 ng/kg iv, PAF caused an increase in Evans blue extravasation of 220% (P less than 0.05) in the trachea, with the greatest effect at a dose of 100 ng/kg (858%; P less than 0.01). Histamine (150 micrograms/kg iv) caused a 320% increase over base line in the trachea and 200% in main bronchi; this effect was equ

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Vezza, Roberta, Anna Mezzasoma, Gigliola Venditti, and Paolo Gresele. "Prostaglandin Endoperoxides and Thromboxane A2 Activate the same Receptor Isoforms in Human Platelets." Thrombosis and Haemostasis 87, no. 01 (2002): 114–21. http://dx.doi.org/10.1055/s-0037-1612953.

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SummaryArachidonic acid (AA) is a potent inducer of platelet aggregation in vitro; this activity is due to its conversion to biologically active metabolites, prostaglandin (PG) endoperoxides and thromboxane A2 (TxA2). PG endoperoxides and TxA2 are thought to act on the same receptor; however, at least two isoforms of this receptor have been identified. The aim of our work was to clarify whether endoperoxides and TxA2 activate the same or different receptor subtypes to induce aggregation and calcium movements in human platelets.AA-induced aggregation and calcium rises were still detectable in p

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Rickard, Alice, Craig Portell, Pamela J. Kell, Suzanne M. Vinson, and Jane McHowat. "Protease-activated receptor stimulation activates a Ca2+-independent phospholipase A2 in bladder microvascular endothelial cells." American Journal of Physiology-Renal Physiology 288, no. 4 (2005): F714—F721. http://dx.doi.org/10.1152/ajprenal.00288.2004.

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Increased mast cell numbers and mast cell activation represent one of the prevalent etiologic theories for interstitial cystitis, an inflammatory condition in the bladder. This study was designed primarily to determine whether increased mast cell tryptase in the bladder wall may play a role in activating bladder endothelial cell phospholipase A2 (PLA2), leading to increased inflammatory phospholipid metabolite accumulation, which may propagate the inflammatory process. We stimulated human bladder microvascular endothelial cells with thrombin or tryptase and measured the activation of PLA2 and

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BUSCHBECK, Marcus, Farideh GHOMASHCHI, Michael H. GELB, Steve P. WATSON, and Angelika G. BÖRSCH-HAUBOLD. "Stress stimuli increase calcium-induced arachidonic acid release through phosphorylation of cytosolic phospholipase A2." Biochemical Journal 344, no. 2 (1999): 359–66. http://dx.doi.org/10.1042/bj3440359.

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Stress stimuli such as free radicals, high osmolarity or arsenite activate stress-activated protein kinases (SAPKs) in a wide variety of cells. In the present study, we have investigated the ability of several stress stimuli to activate SAPKs in platelets and to induce phosphorylation of their substrates. Treatment of human platelets with H2O2 stimulated SAPK2a and its downstream target mitogen-activated protein kinase-activated protein kinase-2 (MAPKAP-K2). Kinase activity reached a maximum after 2-5 min and declined towards basal levels after 15 min. Arsenite caused a steady increase of MAPK

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40

Triggiani, M., A. N. Fonteh, and F. H. Chilton. "Factors that influence the proportions of platelet-activating factor and 1-acyl-2-acetyl-sn-glycero-3-phosphocholine synthesized by the mast cell." Biochemical Journal 286, no. 2 (1992): 497–503. http://dx.doi.org/10.1042/bj2860497.

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Recent studies have demonstrated that inflammatory cells can be divided into two groups depending on the type of 2-acetylated phospholipids [1-radyl-2-acetyl-sn-glycero-3-phosphocholine (GPC)] they produce: those that produce predominantly platelet-activating factor (PAF), and those that produce predominantly its 1-acyl analogue (1-acyl-2-acetyl-GPC; AAGPC) [Triggiani, Schleimer, Warner & Chilton (1991) J. Immunol. 147, 660-666]. The present study has examined the factors that regulate the production of these two molecules in mouse bone marrow-derived mast cells (BMMC). Initial experiments

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41

Zucker, Marjorie L., Susan E. Budd, Lawrence E. Dollar, Steven B. Chernoff, and Raul Altman. "Effect of Diltiazem and Low-Dose Aspirin on Platelet Aggregation and ATP Release Induced by Paired Agonists." Thrombosis and Haemostasis 70, no. 02 (1993): 332–35. http://dx.doi.org/10.1055/s-0038-1649575.

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SummaryThe authors studied the effects of diltiazem, administered alone and together with low-dose aspirin, on the platelet response to paired agonists. After a baseline period, 25 healthy volunteers were given oral diltiazem for 1 week (120, 240, or 360 mg/day), and then crossed over randomly between 1 week on diltiazem plus aspirin (81 mg/day), and 1 week on aspirin (81 mg/day) alone. Platelet function was tested on 2 consecutive days in each period. Synergistic platelet aggregation and ATP release were obtained at baseline using a subthreshold concentration of arachidonic acid combined with

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Saeed, S. A., H. Rasheed, S. Kumar, et al. "New aspects of cyclooxygenase and signalling inhibitors in arachidonic acid (AA) and platelet activating factor (PAF) mediated platelet aggregation." Biochemical Society Transactions 30, no. 5 (2002): A130. http://dx.doi.org/10.1042/bst030a130.

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Rickard, Alice, and Jane McHowat. "Phospholipid metabolite production in human urothelial cells after protease-activated receptor cleavage." American Journal of Physiology-Renal Physiology 283, no. 5 (2002): F944—F951. http://dx.doi.org/10.1152/ajprenal.00072.2002.

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Our laboratory demonstrated previously that stimulation of protease-activated receptors (PARs) on the human urothelial carcinoma cell line RT4 results in activation of a calcium-independent phospholipase A2 (iPLA2), leading to arachidonic acid and PGE2 release. In this study, we have examined PAR activation in normal human urothelial cells (HUR) leading to the production of inflammatory or cytoprotective phospholipid metabolites. The presence of both PAR-1 and PAR-2 on HUR was confirmed by immunoblotting. Stimulation of PAR-1 with thrombin or PAR-2 by tryptase leads to activation of a membrane

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44

Sharan, Sandeep, Poonam Malhotra Kapoor, Minati Choudhury, V. Devagourou, Ujjwal Kumar Choudhury, and Vajala Ravi. "Role of Platelet Function Test in Predicting Postoperative Bleeding Risk after Coronary Artery Bypass Grafting: A Prospective Observational Study." Journal of Cardiac Critical Care TSS 5, no. 02 (2021): 088–96. http://dx.doi.org/10.1055/s-0041-1728978.

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AbstractPatients undergoing cardiac surgery are at risk of excessive bleeding and its associated complications. Excessive bleeding during and after cardiac surgery has an incidence of ~20%. Massive bleeding and subsequent requirement for blood product administration and mediastinal reexploration are associated with significant morbidity and mortality. Postoperative, nonsurgical bleeding in cardiac surgical patients is often multifactorial. Platelet dysfunction, excessive fibrinolysis, hypothermia, preoperative anemia, and deficiency of coagulation factors or their dilution are all suggested et

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Ferrer-Lopez, P., P. Renesto, M. Schattner, S. Bassot, P. Laurent, and M. Chignard. "Activation of human platelets by C5a-stimulated neutrophils: a role for cathepsin G." American Journal of Physiology-Cell Physiology 258, no. 6 (1990): C1100—C1107. http://dx.doi.org/10.1152/ajpcell.1990.258.6.c1100.

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Human platelets can be stimulated by recombinant human fifth component of complement (rhC5a) in the presence of human neutrophils. After challenge with N-formyl-Met-Leu-Phe or rhC5a, concentrated neutrophils release cathepsin G into the supernatant. The concentrations of cathepsin G recovered by titration of the enzymatic activity correlate with the capability of these supernatants to induce platelet stimulation as measured by serotonin release. Cathepsin G purified from neutrophil granules triggered platelet aggregation and serotonin release independent of arachidonic acid metabolites and pla

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Lapointe, D. S., and M. S. Olson. "Platelet-activating Factor-stimulated Hepatic Glycogenolysis Is Not Mediated through Cyclooxygenase-derived Metabolites of Arachidonic Acid." Journal of Biological Chemistry 264, no. 21 (1989): 12130–33. http://dx.doi.org/10.1016/s0021-9258(18)63829-3.

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Chilton, Floyd H., Marc Cluzel, and Massimo Triggiani. "Recent advances in our understanding of the biochemical interactions between platelet-activating factor and arachidonic acid." Lipids 26, no. 12 (1991): 1021–27. http://dx.doi.org/10.1007/bf02536495.

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Baldi, E., C. Falsetti, C. Krausz, et al. "Stimulation of platelet-activating factor synthesis by progesterone and A23187 in human spermatozoa." Biochemical Journal 292, no. 1 (1993): 209–16. http://dx.doi.org/10.1042/bj2920209.

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The presence of platelet-activating factor (PAF) has been demonstrated recently in mammalian spermatozoa, together with evidence for a role of this phospholipid in enhancing sperm motility and fertilizing ability. To investigate whether PAF synthesis and release occurs in human spermatozoa following incubation with stimuli that induce acrosome reaction, spermatozoa were incubated with progesterone and A23187, two known inducers of the exocytotic event. PAF synthesis (remodelling pathway) was assessed by [3H]acetate incorporation into PAF. Treatment of spermatozoa with progesterone and A23187 r

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Küster, L. J., and J. C. Frölich. "Platelet aggregation and thromboxane release induced by arachidonic acid, collagen, ADP and platelet-activating factor following low dose acetylsalicylic acid in man." Prostaglandins 32, no. 3 (1986): 415–23. http://dx.doi.org/10.1016/0090-6980(86)90009-2.

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Canobbio, Ilaria, Stefania Reineri, Fabiola Sinigaglia, Cesare Balduini, and Mauro Torti. "A role for p38 MAP kinase in platelet activation by von Willebrand Factor." Thrombosis and Haemostasis 91, no. 01 (2004): 102–10. http://dx.doi.org/10.1160/th03-02-0083.

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SummaryPlatelet activation induced by von Willebrand factor (VWF) binding to the membrane GPIb-IX-V receptor involves multiple signal transduction pathways. Among these, recruitment and activation of the FcγRIIA and stimulation of phospholipase A2 represent independent events equally essential to support a complete platelet response. Phospholipase A2 is activated by calcium and by phosphorylation through MAP kinases. In this work, we found that VWF stimulated the rapid and sustained phosphorylation of p38 MAP kinase (p38MAPK). In vitro kinase assay revealed that VWF-stimulated phosphorylation

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