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

Abstract

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.

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

“…In a previous paper, we demonstrated that PAF induced platelet adhesion to endothelial cell surfaces only in the presence of PMNs in vitro (Hirafuji & Shinoda, 1991a). In the present study, to determine whether PMNs release or generate any factor(s) capable of inducing platelet adhesion, the effects of various cell-free preparations from PMNs on platelet adhesion were first examined.…”

“…Endothelial cells, platelets and PMNs were prepared as described previously (Hirafuji & Shinoda, 1991a). In brief, endothelial cells were isolated from human umbilical cord veins by collagenase digestion.…”

“…(Ashida et al, 1983), or indomethacin (3 JAM). However, both superoxide dismutase (SOD; 300 u ml-') and catalase (1000 u ml-') significantly (P< PAF induces platelet adhesion to endothelial cells when intact PMNs were coincubated (Hirafuji & Shinoda, 1991a). The effects of various inhibitors and scavengers of active oxygens were also evaluated on PAF-induced platelet adhesion to endothelial cells in the presence of intact PMNs ( Table 2).…”

“…In a previous report, we demonstrated that platelet-activating factor (PAF) induced platelet adhesion to endothelial cells in the presence of PMNs in vitro, and had no effect in the absence of PMNs (Hirafuji & Shinoda, 1991a). Another potent PMN activator, N-formyl-methionyl-leucyl-phenylalanine also induced platelet adhesion to endothelial cells when PMNs were present, while leukotriene B4 had no effect, suggesting that the induction of platelet adhesion is not a general property of PMN activators (Hirafuji & Shinoda, 1991b).…”

Involvement of thromboxane A2 and tyrosine kinase in the synergistic interaction of platelet activating factor and calcium ionophore A23187 in human platelet aggregation

“…It also induces adhesion of platelets to the endothelium in the presence of activated leukocytes (Hirafuji and Shinoda, 1991). PAF is also known to play an important role in various pathophysiological conditions that include modulation of blood pressure, hypotension, cardiac dysfunction, cardiac anaphylaxis, hemorrhagic, traumatic and septic shock syndromes (Anderson et al, 1991;Montrucchio et al, 2000).…”