Abstract
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.
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Selected References
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