Nomura S, Nagata H, Yanabu M, Suzuki M, Soga T, Ohga S, Kondo K, Sone N, Kitada C, Kitajima H
Nihon Ketsueki Gakkai Zasshi. 1989 Aug;52(5):895-905.
We used flow cytometry to investigate the change of platelet membrane glycoproteins (GPIb and GP IIb/IIIa) and the distributions of fibrinogen (Fbg), thrombospondin (TSP) and fibronectin (Fn) on the surface of thrombin-stimulated platelets. The binding of a monoclonal antibody directed at the von Willebrand factor binding site on GPIb decreased in thrombin-stimulated platelets. This antibody caused a reactive delay in thrombin-induced aggregation, but had little influence on aggregability. Slight thrombin-induced aggregation was observed even after blocking the binding of Fbg to GP II b/IIIa. The new expression of GP II b/IIIa was detected on the surface of thrombin-stimulated platelets, whereas there was little increase of Fbg dependent on this GP II b/IIIa. An increase of TSP after thrombin stimulation was observed on the surface of platelets of healthy controls and patients with Glanzmann's thrombasthenia (Type I). The level of on platelet surface was slightly increased by thrombin stimulation. The mechanism involved in thrombin-induced aggregation appears to differ from that in ADP-induced aggregation.
我们采用流式细胞术研究凝血酶刺激的血小板表面血小板膜糖蛋白（糖蛋白 Ib 和糖蛋白 IIb/IIIa）的变化以及纤维蛋白原（Fbg）、血小板反应蛋白（TSP）和纤连蛋白（Fn）的分布情况。针对糖蛋白 Ib 上血管性血友病因子结合位点的单克隆抗体在凝血酶刺激的血小板中的结合减少。该抗体在凝血酶诱导的聚集过程中导致反应延迟，但对聚集性影响不大。即使在阻断 Fbg 与糖蛋白 IIb/IIIa 的结合后，仍观察到轻微的凝血酶诱导聚集。在凝血酶刺激的血小板表面检测到糖蛋白 IIb/IIIa 的新表达，而依赖于该糖蛋白 IIb/IIIa 的 Fbg 几乎没有增加。在健康对照者和 I 型血小板无力症患者的血小板表面观察到凝血酶刺激后 TSP 增加。血小板表面的水平因凝血酶刺激而略有增加。凝血酶诱导聚集所涉及的机制似乎与 ADP 诱导聚集的机制不同。
