Antagonism of Platelet-Activating Factor-Induced Increase in Cytosolic Free Calcium Concentration in Human Endothelial Cells.

Hirafuji, Masahiko; Satoh, Hisashi

doi:10.1254/jjp.58.231

Cited by 5 publications

(2 citation statements)

References 27 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. However, PAF alone at a concentration (10nM) that induces full aggregation did not induce platelet adhesion even to the thrombogenic endothelial cells without the sonicates, suggesting that some factor(s) in the sonicates are prerequisite to the ultimate platelet-endothelial cell interactions.…”

Section: Discussionmentioning

confidence: 99%

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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: 99%

“…(6-keto-PGFI.) by a specific radioimmunoassay (Hirafuji & Shinoda, 1992 -cyclopentyl-16, 17, 18, 19, 20-pentanor-prostaglandin I2ua-cyclodextrin clathrate), 6-keto-PGFI,. and its antiserum were also kindly provided by Ono Pharmaceuticals Indust., Ltd., Japan.…”

Section: Determination Ofprostacyclinmentioning

confidence: 99%

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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Platelet-activating factor–induced calcium mobilization and oxidative metabolism in hepatic macrophages and endothelial cells

Gardner

Laskin

1993

Journal of Leukocyte Biology

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Fluorescence image analysis of the calcium sensitive dye Indo-1 was used to characterize platelet-activating factor (PAF)-induced calcium mobilization in hepatic macrophages and endothelial cells. PAF, but not lyso-PAF, an inactive analog, induced a rapid and transient increase in intracellular levels of calcium that appeared to depend on the presence of extracellular calcium. In both macrophages and endothelial cells, these effects were dose dependent, reaching maximal levels with 10 nM PAF. However, the kinetics of the calcium response to PAF in macrophages and endothelial cells was distinct. The endothelial cells responded more rapidly to PAF than the macrophages (within 1 min vs. 2-3 min, respectively) and displayed longer recovery periods (4 min vs. > 10 min, respectively). In contrast, the magnitude of the response to PAF was greater in the macrophages. In both cell types, triazolam and alprazolam, two PAF antagonists, and the calcium channel blocker verapamil inhibited PAF-induced calcium mobilization. PAF also stimulated superoxide anion production alone and in combination with the macrophage activator 12-O-tetradecanoyl-phorbol-13-acetate (TPA) in both cell types. Macrophages produced more of this reactive oxygen intermediate in response to PAF and TPA than endothelial cells. Interestingly, in the absence of extracellular calcium or when verapamil was added to the cultures, superoxide anion production by the macrophages, but not the endothelial cells, was significantly reduced. These results demonstrate that, although hepatic macrophages and endothelial cells mobilize calcium in response to PAF, the characteristics of the response in each cell type are different. These differences may underlie, at least in part, distinct functional responses of the cells to PAF.

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5-Hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels in rat vascular smooth muscle cells

Hirafuji

Kawahara

Ebihara

et al. 1999

European Journal of Pharmacology

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Antagonism of Platelet-Activating Factor-Induced Increase in Cytosolic Free Calcium Concentration in Human Endothelial Cells.

Cited by 5 publications

References 27 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

Platelet-activating factor–induced calcium mobilization and oxidative metabolism in hepatic macrophages and endothelial cells

5-Hydroxytryptamine induces transient Ca2+ influx through Ni2+-insensitive Ca2+ channels in rat vascular smooth muscle cells

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