Fiedel B A
Division of Immunology, James N. Gamble Institute of Medical Research, Cincinnati, Ohio 45219.
Immunology. 1988 Jan;63(1):169-70.
Fibrinogen augmented gel-filtered platelet (GFP) aggregation only during an intermediate level of platelet activation stimulated by aggregated C-reactive protein (CRP) (AggCRP), implying that a mechanism to utilize fibrinogen is not operative or does not require an exogenous source of fibrinogen at near-maximal or threshold levels of platelet activation. By contrast, inclusion of the tetrapeptide fibrinogen antagonist, Arg-Gly-Asp-Ser(RGDS), inhibited both intermediate and near-maximal, but not threshold, levels of platelet activation stimulated by AggCRP. These data suggest that AggCRP initially stimulates platelets independent of fibrinogen but, in so doing, activates a fibrinogen-dependent mechanism(s) capable of augmenting the overall extent of platelet stimulation.
纤维蛋白原仅在聚集的C反应蛋白(AggCRP)刺激的血小板活化的中间水平增强凝胶过滤血小板(GFP)聚集,这意味着在血小板活化的接近最大或阈值水平时,利用纤维蛋白原的机制不起作用或不需要外源纤维蛋白原。相比之下,包含四肽纤维蛋白原拮抗剂Arg-Gly-Asp-Ser(RGDS)可抑制AggCRP刺激的血小板活化的中间水平和接近最大水平,但不抑制阈值水平。这些数据表明,AggCRP最初独立于纤维蛋白原刺激血小板,但这样做会激活一种能够增强血小板刺激总体程度的纤维蛋白原依赖性机制。