Transient increase of cytosolic free calcium in cultured human vascular endothelial cells by platelet-activating factor

Hirafuji, Masahiko; Maeyama, Kazutaka; Watanabe, Takehiko; Ogura, Yasumi

doi:10.1016/0006-291x(88)90226-4

Cited by 37 publications

(21 citation statements)

References 18 publications

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“…The increased binding of PMNs induced by treatment of EC with PAF could have been due to interaction of PAF localized on the EC surface with the neutrophils, or to activation of the ECs by PAF (Bussolino et al, 1987b;Hirafuji et al, 1988), causing them to express a second adhesive molecule. To differentiate between these two possibilities, we preti'eated ECs with PAF and then incubated the monolayers with AH, or with control buffer, before adding PMNs and measuring their adhesion (Fig.…”

Section: Paf In Liposomes and Associated With The Ec Surface Induces mentioning

confidence: 99%

Endothelial cell-associated platelet-activating factor: a novel mechanism for signaling intercellular adhesion.

Zimmerman

McIntyre

Mehra

et al. 1990

The Journal of Cell Biology

358

153

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Abstract. The binding of neutrophils (polymorphonuclear leukocytes [PMNs]) to endothelial cells (ECs) presents special requirements in the regulation of intercellular adhesion. ECs that are stimulated by certain agonists, including thrombin and cytokines (tumor necrosis factor or, interleukin-1), generate molecular signals that induce the adhesion of PMNs (endothelial cell-dependent neutrophil adhesion). Our experiments demonstrate that the mechanism of binding induced by thrombin is distinct from that induced by the cytokines based on the time courses, the requirement for protein synthesis, and differential binding of HL60 promyelocytic leukemia cells to ECs activated by the two classes of agonists. The rapid EC-dependent PMN adhesion (initiated in minutes) that occurs when the ECs are stimulated by thrombin is temporally coupled with the accumulation of platelet-activating factor, a biologically active phosphoglyceride that remains associated with ECs and that activates PMNs by binding to a cell surface receptor. A portion of the newly synthesized plateletactivating factor (PAF) is on the EC surface, as demonstrated by experiments in which the rate of hydrolysis of PAF synthesized by activated ECs was accelerated by extracellular PAF acetylhydrolase. When ECs were treated with exogenous PAF they became adhesive for PMNs; the PMN binding was prevented by incubating the ECs with PAF acetylhydrolase or by treating the PMNs with competitive PAF receptor antagonists. Thus PAF associated with the EC plasma membrane induces PMN binding, an observation supported by experiments in which PAF in model membranes (liposomes) stimulated rapid PMN adhesion to ECs and to cell-free surfaces. In addition, competitive antagonists of the PAF receptor inhibited the binding of PMNs to ECs activated by thrombin and other rapidly acting agonists, but not to ECs activated by tumor necrosis factor c~, indicating that PAF that is endogenously synthesized by ECs can mediate neutrophil adhesion. These experiments demonstrate a novel mechanism by which a cell-associated phospholipid, PAF, can serve as a signal for an intercellular adhesive event.

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Section: Paf In Liposomes and Associated With The Ec Surface Induces mentioning

confidence: 99%

Endothelial cell-associated platelet-activating factor: a novel mechanism for signaling intercellular adhesion.

Zimmerman

McIntyre

Mehra

et al. 1990

The Journal of Cell Biology

358

153

View full text Add to dashboard Cite

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“…These results suggest that the platelet adhesion is mediated by activation of PAF specific membrane receptors, most probably on PMNs. However, PAF is an activator not only of platelets but also of endothelial cells (Bussolino et al, 1987;Hirafuji et al, 1988) so a possibility remains that the simultaneous PAF activation of platelets and/or endothelial cells as well as PMNs is a prerequisite to the platelet adhesion.…”

Section: Discussionmentioning

confidence: 99%

Platelet‐leukocyte interaction in adhesion to endothelial cells induced by platelet‐activating factor in vitro

Hirafuji

Satoh

1991

British J Pharmacology

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1 Platelet-activating factor (PAF, 10 nM) did not induce platelet adhesion to endothelial cells cultured in monolayer but it induced their adhesion to protein-coated plastic. However, PAF induced a marked platelet adhesion to endothelial cells when polymorphonuclear leukocytes (PMNs) were present. Lyso-PAF had no effect. 2 Phase-contrast microscopic examination showed that single platelets rather than their aggregates adhered to the endothelial cell surface around aggregating and adhering PMNs. 3 Significant platelet adhesion was induced by PAF at concentrations higher than 0.01 nm with the maximal response at 10nm. Platelet adhesion occurred within minutes after PAF addition, reaching a maximum approximately after 30 min. Platelet adhesion also occurred significantly at a PMN : platelet ratio of 1: 800, and linearly up to 1: 50. 4 The PAF-induced platelet adhesion was suppressed by three structurally unrelated PAF antagonists, WEB 2086, ONO 6240 and BN 52021, in a concentration-dependent manner. 5 PAF also increased PMN adhesion to endothelial cell monolayers, which was further augmented by the presence of platelets. 6 The present study demonstrates that PAF induces platelet adhesion to endothelial cells in vitro when PMNs are present and that there is a close interaction between platelets and PMNs in their adhesion to endothelial cells. The present study further suggests that PMNs could play a central role in platelet adhesion to vascular endothlium in certain pathological conditions.

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“…However, despite the multiple functional re sponses evoked by PAF in endothelial cells as described above and possible therapeutic advantage of the antagonists, few studies have been made to evaluate the potency of PAF antagonists in endothelial cells. In a previous report, we showed that PAF increased cytoso lic free calcium concentration, [Ca 21]i, in hu man endothelial cells cultured in monolayer by a continuous superfusion technique using a calcium fluorescence dye, fura-2 (9). An in crease in [Ca 21]i is an essential initial event coupled to cell activation.…”

mentioning

confidence: 91%

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

Hirafuji

Satoh

1992

Jpn.J.Pharmacol

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ABSTRACT-The effects of platelet-activating factor (PAF) antagonists on the agonist-induced increase in cytosolic free calcium concentration, [Ca 2+]i, in human vascular endothelial cells grown in monolayer were investigated by a continuous su perfusion technique using a calcium fluorescent probe, fura-2. PAF caused a small but dose-dependent increase in [Ca 2+];. Seven structurally dissimilar PAF antagonists dose-dependently suppressed the peak response, among which WEB 2086 was the most potent, followed by WEB 2170 > FR 900452 ONO 6240 > BN 52021 kad surenone CV 3988. These antagonists except for CV 3988 were specific for PAF, since they had no effects on calcium mobilization induced by thrombin or histamine, while CV 3988 had a non-specific effect. PAF in the same range of concentration in creased prostacyclin release from human endothelial cells. WEB 2086 also inhibited the PAF-induced prostacyclin release, while it had no effect on the release induced by histamine and thrombin. These results demonstrate the specificity and dose-response characteristics of PAF antagonists in cultured human endothelial cells and suggest that a PAF antagonist could be a valuable therapeutic agent in certain human diseases where PAF activation of endothelial cells may have a critical role.

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Transient increase of cytosolic free calcium in cultured human vascular endothelial cells by platelet-activating factor

Cited by 37 publications

References 18 publications

Endothelial cell-associated platelet-activating factor: a novel mechanism for signaling intercellular adhesion.

Endothelial cell-associated platelet-activating factor: a novel mechanism for signaling intercellular adhesion.

Platelet‐leukocyte interaction in adhesion to endothelial cells induced by platelet‐activating factor in vitro

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

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