Fibrinogen and thrombospondin play a major role in the molecular mechanism of interplatelet recognition during aggregation.
In previous studies it was shown that fixed platelets bearing covalently-bound fibrinogen participate passively in release-related aggregation, and that thrombospondin is the released compound which specifically and selectively recognizes the affixed fibrinogen. The present study demonstrates that the phenomenon of passive participation is also obtained with fixed platelets bearing covalently-bound thrombospondin. Moreover, a full resolution and reconstitution of interplatelet recognition during aggregation was obtained with two different systems: (a) fixed platelets bearing affixed fibrinogen were caused to aggregate when stirred and supplemented with soluble thrombospondin; (b) fixed platelets bearing fibrinogen and fixed platelets bearing thrombospondin, each uncapable of undergoing aggregation, aggregated when combined and stirred. It is concluded that fibrinogen and thrombospondin play a major role in the molecular mechanism of interplatelet recognition during aggregation.
No takes yet. Share an insight, caveat, or question.
Agam et al. (1988) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: