The role of fibronectin in platelet adhesion to plasma preadsorbed polystyrene
The role of fibronectin in platelet adhesion to plasma preadsorbed polystyrene
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DOI：
10.1163/156856299x00117
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发表时间：
1999-01-01
影响因子：
3.6
通讯作者：
Horbett, TA
中科院分区：
文献类型：
--
作者：
Tsai, WB;Horbett, TA
血小板对与血液接触的合成表面的粘附是通过粘附血浆蛋白（尤其是纤维蛋白原）的吸附介导的。然而，其他粘附蛋白，例如纤连蛋白、玻连蛋白和冯维勒布兰德因子在血小板粘附中的作用尚不清楚。在这项研究中，使用三种方法评估了纤连蛋白在血小板粘附到表面中的作用。首先，在用纤连蛋白耗尽的血浆预吸附的Immulon I(R)或用增加量的纤连蛋白补充的纤连蛋白耗尽的血浆上测量血小板粘附力。在这些条件下，从血浆中吸附的纤连蛋白对血小板粘附没有任何影响，而纤维蛋白原在介导血小板粘附中起主要作用。由于纤连蛋白可能在血小板粘附到很少或不吸附纤维蛋白原的表面上发挥作用；我们还使用了另外两种策略来评估纤连蛋白的潜在作用。一种是使用经过血小板活化抑制剂前列腺素 E-1 处理的血小板，该抑制剂可防止血小板纤维蛋白原受体 GP IIb/IIIa 的活化。经前列腺素E-1处理的血小板与血浆预吸附的Immulon IO的粘附力与未处理的血小板相比大大降低，但通过向血浆中添加超常浓度的纤连蛋白而增加。这表明GP Ic/IIa，而不是GP IIb/IIIa，可能是负责血小板粘附到表面结合纤连蛋白的血小板受体。最后，我们研究了纤连蛋白对血小板粘附到用纤连蛋白耗尽的无纤维蛋白原血浆预吸附的表面的影响。我们发现纤连蛋白重新添加到纤连蛋白耗尽的无纤维蛋白原血浆中可增加血小板粘附。然而。我们最重要的结论是，纤连蛋白似乎在介导血小板粘附到用正常血浆预吸附的聚苯乙烯表面方面发挥很小或没有作用。
Platelet adhesion to synthetic surfaces that come in contact with blood is mediated by the adsorption of adhesive plasma proteins, especially fibrinogen. However, the roles of other adhesive proteins, such as fibronectin, vitronectin: and von Willebrand factor in platelet adhesion are not yet clear. In this study, the role of fibronectin in platelet adhesion to surfaces was assessed using three approaches. First, platelet adhesion was measured on Immulon I(R) preadsorbed with fibronectin-depleted plasma or fibronectin-depleted plasma replenished with increasing amount of fibronectin. Under these conditions, fibronectin adsorbed from plasma did not have any effect on platelet adhesion, while fibrinogen played a major role in mediating platelet adhesion. Since fibronectin might play a role in platelet adhesion to surfaces which adsorb little or no fibrinogen; we also used two other strategies to assess the potential role of fibronectin. One was to use platelets treated with a platelet activation inhibitor, prostaglandin E-1, which prevents the activation of platelet fibrinogen receptor GP IIb/IIIa. The adhesion of prostaglandin E-1-treated platelets to Immulon IO preadsorbed with plasma was greatly decreased compared to that of untreated platelets, but was increased by the addition of supernormal concentrations of fibronectin to the plasma. This suggests that GP Ic/IIa, rather than GP IIb/IIIa, might be the platelet receptor which is responsible for platelet adhesion to surface-bound fibronectin. Finally, we studied the effect of fibronectin on platelet adhesion to surfaces preadsorbed with fibronectin-depleted afibrinogenemic plasma. We found that fibronectin re-addition to fibronectin-depleted afibrinogenemic plasma increased platelet adhesion. However. our most important Ending was that fibronectin seems to play little or no role is mediating platelet adhesion to polystyrene surfaces preadsorbed with normal plasma.