Activities of enzymes that metabolize platelet-activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) in neutrophils and eosinophils from humans and the effect of a calcium ionophore

Lee, Ten-ching; Malone, Boyd; Wasserman, Stephen I.; Fitzgerald, Veronica; Snyder, Fred

doi:10.1016/0006-291x(82)90928-7

Cited by 178 publications

(30 citation statements)

References 24 publications

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“…This result indicates that the sonicates contain PAF which was not inactivated by acetylhydrolase (Lee et al, 1982), and that platelet adhesion to thrombogenic endothelial cells requires, at a minimum, the activation of both, or either, the platelets and/or endothelial cells by PAF. Since PAF is a potent agonist in rabbit platelets and a weak agonist in human endothelial cells (Hirafuji & Shinoda, 1992), platelets may be the target cells of PAF.…”

Section: Discussionmentioning

confidence: 81%

Roles of prostacyclin, EDRF and active oxygens in leukocyte‐dependent platelet adhesion to endothelial cells induced by platelet‐activating factor in vitro

Hirafuji

Satoh

1993

British J Pharmacology

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The mechanism of polymorphonuclear leukocyte (PMN)‐dependent platelet adhesion to cultured endothelial cells induced by platelet‐activating factor (PAF) was investigated to determine whether PMNs release or generate any factor(s) capable of inducing platelet adhesion, and the roles of prostacyclin and endothelium‐derived relaxing factor (EDRF). Cell‐free supernatants, sonicates or rapid filtrates of PAF‐stimulated PMN suspensions did not induce platelet adhesion to endothelial cells, but the PMN sonicates induced platelet adhesion when endothelial cells were pretreated with both aspirin and NG‐nitro‐lm‐arginine (l‐NOARG). Its microphotograph showed that mainly platelet aggregates adhered to the endothelial cell surface. Platelet adhesion induced by the PMN sonicates to aspirin‐ and l‐NOARG‐pretreated endothelial cells was dose‐dependently prevented by OP‐41483 (1–100 nm), and slightly by l‐arginine (1 mm). The inhibition of platelet adhesion by OP‐41483 and l‐arginine was potentiated by their combination. WEB 2170 (3 μm), a PAF antagonist, inhibited platelet adhesion induced by the PMN sonicates. However, PAF alone did not induce significant platelet adhesion to aspirin‐ and l‐NOARG‐treated endothelial cells. Platelet adhesion induced by the PMN sonicates was not suppressed by AA‐861 and indomethacin. However, both superoxide dismutase and catalase significantly inhibited platelet adhesion, and, in combination, their inhibitory effect was synergistically potentiated. Mannitol had no effect. It was also significantly inhibited by α1‐antitrypsin, whereas chymostatin and elastatinal had no effect. PAF‐induced platelet adhesion to endothelial cells in the presence of intact PMNs was not suppressed by indomethacin and AA‐861, or by protease inhibitors. SOD alone, and in combination with catalase, caused a slight but significant inhibition, while catalase and mannitol by themselves had no effect. PMN‐induced platelet adhesion was slightly inhibited by OP‐41483 (100 nm). l‐Arginine (1 mm) alone had no effect, but slightly potentiated the effect of OP‐41483. This platelet adhesion was not accompanied by suppression of prostacyclin synthesis. The results with the PMN sonicates show that prostacyclin, EDRF and active oxygens are important modulators of intercellular interactions between platelets and endothelial cells. These results further suggest that the mechanism of intact PMN‐dependent platelet adhesion is primarily through platelet‐endothelial cell interactions in which leukocyte‐derived active oxygens play a role, but does not involve platelet‐platelet interactions inhibitable by prostacyclin.

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Section: Discussionmentioning

confidence: 81%

Roles of prostacyclin, EDRF and active oxygens in leukocyte‐dependent platelet adhesion to endothelial cells induced by platelet‐activating factor in vitro

Hirafuji

Satoh

1993

British J Pharmacology

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“…Stimulation of human and animal eosinophils with various soluble and nonsoluble agents leads to the formation of various arachidonic acid-derived lipids, including LTC 4 [63,69,[115][116][117], PGE [118,119], prostaglandin F 1 (PGF 1 ) and TxA 2 [64,[119][120][121][122][123], PGD 2 and prostaglandin F 2α (PGF 2α ) [64,123]. In addition, eosinophils have been shown to synthesize large amounts of PAF [117,[124][125][126].…”

Section: Oxygen Metabolitesmentioning

confidence: 99%

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

Kroegel¹,

Virchow²,

Luttmann³

et al. 1994

Eur Respir J

129

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P Pu ul lm mo on na ar ry y i im mm mu un ne e c ce el ll ls s i in n h he ea al lt th h a an nd d d di is se ea as se e: : t th he e e eo os si in no op ph hi il l l le eu uc co oc cy yt te e ( (P Pa ar rt t I I) ) ABSTRACT: Increasing evidence has accumulated to suggest that eosinophils play a key role in the pathogenesis of asthma and other pulmonary diseases by damaging infiltrated bronchial tissue and lung parenchyma. The first part of this review on eosinophils describes the cellular characteristics and properties of the cell, which help in understanding its role in disease. The article focuses on origin, maturation and differentiation of the eosinophil, its morphological and phenotypical properties, as well as its preformed and newly generated mediators of inflammation. The cause and putative significance of eosinophil heterogeneity in respect to function and density will also be discussed. In addition, the naturally occurring mediators through which eosinophils are activated and communicate with other inflammatory cells are outlined.The first part closes with new aspects of eosinophil recruitment from the circulation into perivascular tissue, including nonselective and putative selective adhesion mechanisms and chemotaxis.

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“…It has been reported that the activity of PAF acetylhydrolase was elevated in eosinophils obtained from patients with eosinophilia and could be stimulated severalfold in neutrophils by ionophore A23187 (25). The acetylhydrolase activity was also elevated in plasma of spontaneously hypertensive rats (19) and in serum of white males who had hypertension (26).…”

mentioning

confidence: 98%

Platelet-activating factor acetylhydrolase activity in maternal, fetal, and newborn rabbit plasma during pregnancy and lactation.

Maki

Hoffman

Johnston

1988

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

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The inactivation of the biologically active ether-containing glycerophospholipid platelet-activating factor (PAF) is catalyzed by the enzyme PAF acetylhydrolase (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetylhydrolase, EC 3.1.1.48). The specific activity of acetylhydrolase has been assayed in maternal rabbit plasma prior to and throughout pregnancy and after parturition. The specific activity of acetylhydrolase was 131 + 8 nmol-min -'ml'-of plasma (mean ± SEM) in the nonpregnant rabbit. Similar specific activities were found throughout the first half of pregnancy; however, on day 15 the acetylhydrolase activity began to decrease and reached a minimum around day 27. Within 24-48 hr following delivery, the specific activity of the enzyme increased to the levels found in the nonpregnant animals. The specific activity of acetylhydrolase in fetuses (gestational ages of 21-30 days) and neonates increased from 22 nmol min'-1 ml-1 of plasma (21-day-old) to 328 nmolinin ml' of plasma (35-day-old rabbits). The decrease in enzymatic activity of the pregnant rabbit plasma cannot be accounted for by the presence of an inhibitor as determined by plasma-mixing experiments with nonpregnant and pregnant (27-day) plasma. The properties of this enzyme in the rabbit were consistent with those reported by others, i.e., substrate specificity, inactivation by heat and various inhibitors, and Ca2" inde-

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Activities of enzymes that metabolize platelet-activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) in neutrophils and eosinophils from humans and the effect of a calcium ionophore

Cited by 178 publications

References 24 publications

Roles of prostacyclin, EDRF and active oxygens in leukocyte‐dependent platelet adhesion to endothelial cells induced by platelet‐activating factor in vitro

Roles of prostacyclin, EDRF and active oxygens in leukocyte‐dependent platelet adhesion to endothelial cells induced by platelet‐activating factor in vitro

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

Platelet-activating factor acetylhydrolase activity in maternal, fetal, and newborn rabbit plasma during pregnancy and lactation.

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