1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet-activating factor) stimulates calcium influx in rabbit platelets

Lee, Ten-ching; Malone, Boyd; Blank, Merle L.; Snyder, Fred

doi:10.1016/s0006-291x(81)80147-7

Cited by 91 publications

(22 citation statements)

References 19 publications

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“…These results indicate that the influx of extracellular Ca 2+ is essential for PAF-induced platelet activation in dogs, as Lee et al reported for rabbit platelets [12]. Mobilization of intracellular Ca 2+ may also be involved in the PAF-induced response because cytosolic Ca 2+ was mildly increased by PAF under the decalcified conditions described above, but this small increase of Ca 2+ is unlikely to be sufficient to induce platelet aggregation.…”

supporting

confidence: 72%

“…Before an effective therapy to prevent or minimize the platelet activation in endotoxemia can be developed, the mechanism of the reactions must be investigated. Because LPS alone does not induce platelet activation in vitro [4,12], it is predicted that another mediator plays an important role in platelet activation in animals with endotoxemia. Jarvis and Evans reported that LPS induces equine platelet aggregation in whole blood and that platelet activating factor (PAF) released by neutrophils mediates this reaction [8].…”

mentioning

confidence: 99%

“…Lee et al reported that the influx of extracellular Ca 2+ via Ca 2+ channels is the most important factor in PAF induced platelet activation in rabbits [12]. Increased cytosolic Ca 2+ forms a complex with calmodulin and this complex triggers myosin light chain kinase activation [15].…”

mentioning

confidence: 99%

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Characterization of Canine Platelet Activation Induced by Platelet Activating Factor (PAF)

Tsuchiya

Tatsuki

Kitao³

et al. 2008

The Journal of Veterinary Medical Science

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ABSTRACT. Characteristics of the signal transduction in Platelet activating factor (PAF)-activated platelets and effects of anti-platelet agents on this response were investigated in vitro for potential therapeutic applications in canine endotoxemia. Blockade of the PAF receptor by a specific blocker has the strongest inhibitive effect on the PAF-induced platelet reactions. The response was also inhibited by either Ca 2+ channel blockers or prostaglandin E 1 .KEY WORDS: canine platelet, inhibitor, platelet activating factor.

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confidence: 99%

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Characterization of Canine Platelet Activation Induced by Platelet Activating Factor (PAF)

Tsuchiya

Tatsuki

Kitao³

et al. 2008

The Journal of Veterinary Medical Science

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“…PAF elicits physiological responses by increasing the intracellular concentration of Ca2+ (24). But, unlike PtdOH, it exhibits no ionophoretic properties in intact lipid bilayers (32).…”

Section: Discussionmentioning

confidence: 99%

“…These biochemical responses are induced also by other platelet stimuli such as ADP, thrombin, or ionophore A23187 (19)(20)(21) and are thought to be the consequence of the release of Ca2" from a cellular pool inaccessible to chelating agents (20,22,23). Direct studies suggest that PAF induces a rapid mobilization of Ca2" in platelets (24).…”

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confidence: 99%

Platelet-activating factor stimulates metabolism of phosphoinositides in horse platelets: possible relationship to Ca2+ mobilization during stimulation.

Billah¹,

Lapetina²

1983

Proc. Natl. Acad. Sci. U.S.A.

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Stimulation of horse platelets with platelet-activating factor (PAF) induces a rapid degradation of phosphatidylinositol 4,5-bisphosphate [Ptdlns(4,5)P2j. Addition of 0.1 JM PAF for 5 sec to platelets prelabeled with 32P induces a 50% loss of [32P]Ptdlns(4,5)P2. 32P-Labeled phosphatidylinositol 4-monophosphate (PtdIns4P) and [32P]phosphatidylinositol (PtdIns) also are decreased, albeit at a slower rate. Loss Of 32P radioactivity correlates with a net loss of fatty acids from both polyphosphoinositides. Stimulation of platelets with PAF also produces formation of [32P]phosphatidic acid and [32P]lysophosphatidylinositol. The initial disappearance of inositol lipids is subsequently followed by resynthesis, as evidenced by increased incorporation of 32p into Ptdlns(4,5)P2, PtdIns4P, and PtdIns. The resynthesis of the inositides increases with time and is proportional to the concentration of PAF. Prostacyclin (1 ,uM) inhibits (i) the formation of phosphatidic acid and lysophosphatidylinositol and (ii) the resynthesis of polyphosphoinositides induced by 0.03 ,uM PAF without affecting the initial loss of Ptdlns(4,5)P2. The loss of inositol lipids appears to be a primary event of platelet activation. The initial loss of polyphosphoinositides might be linked to the initiation of cellular activation by mobilizing membrane-bound Ca2+, whereas the subsequent formation of these lipids might be involved in mechanisms to prevent overstimulation of the cell.Platelet-activating factor (PAF), a phospholipid mediator of anaphylaxis (1), is released from leucocytes after immunologic and nonimmunologic stimulation (2). The structure of this compound has been elucidated as 1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (3, 4). PAF induces hypotension (5, 6), neutropenia, and thrombocytopenia in vivo (7,8); in vitro, PAF promotes chemotaxis and degranulation in neutrophils (9-11) and induces shape change, release of granule content, and aggregation in platelets (12)(13)(14)(15)(16).The biochemical mechanisms by which PAF elicits physiological responses are not fully understood. In platelets, PAF has been shown to stimulate the phosphatidylinositol (PtdIns) cycle (16, 17), release of arachidonic acid from membrane phospholipids (16,18), and the phosphorylation of specific proteins (10). These biochemical responses are induced also by other platelet stimuli such as ADP, thrombin, or ionophore A23187 (19)(20)(21) and are thought to be the consequence of the release of Ca2" from a cellular pool inaccessible to chelating agents (20,22,23 The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact. platelets (25). Because PtdIns(4,5)P2 might provide Ca2+-binding sites in the plasma membrane (26-28), it has been suggested that the rapid loss of this phospholipid might be a mechanism by which the initial release of Ca2+ could be achieved (25). We now show that PAF also causes a ra...

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Composition of ether‐linked sub‐classes of glycerophospholipids in clones with a different metastatic potential isolated from a murine fibrosarcoma line (T3 cells)

Fallani

Mannori

Ruggieri

1995

Intl Journal of Cancer

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An increase of ether-linked sub-classes of choline and ethanolamine glycerophospholipids has been shown in different types of tumor cells, and correlated with some of their specific biological parameters. In the present study, we examined the composition of ether-linked lipids in a series of clones with a different lung-colonizing potential isolated in our laboratory from a highly metastatic fibrosarcoma line (T3 cells). We found good correlation between the metastatic potential of T3 isolates and increased proportions of both alkylacyl and alkenylacyl subclasses in choline glycerophospholipids (CGP). Moreover, propagation of a weakly metastatic T3 clone in tissue culture led to the emergence of a sub-clone which expressed high metastatic potential together with a high level of alkylacyl and alkenylacyl CGP. No differences were found in the alkylacyl and alkenylacyl-ethanolamine glycerophospholipids (EGP) between the strongly and weakly metastatic T3 clones. We discuss the accumulation of alkylacyl and alkenylacyl CGP in metastatic cells for its possible role in metastatic diffusion by generation of platelet-activating factor (PAF).

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1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet-activating factor) stimulates calcium influx in rabbit platelets

Cited by 91 publications

References 19 publications

Characterization of Canine Platelet Activation Induced by Platelet Activating Factor (PAF)

Characterization of Canine Platelet Activation Induced by Platelet Activating Factor (PAF)

Platelet-activating factor stimulates metabolism of phosphoinositides in horse platelets: possible relationship to Ca2+ mobilization during stimulation.

Composition of ether‐linked sub‐classes of glycerophospholipids in clones with a different metastatic potential isolated from a murine fibrosarcoma line (T3 cells)

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