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Comment
. 2000 Mar;105(6):699-701.
doi: 10.1172/JCI9604.

Old concepts and new developments in the study of platelet aggregation

Z M Ruggeri  1
Affiliations
Comment

Old concepts and new developments in the study of platelet aggregation

Z M Ruggeri. J Clin Invest. 2000 Mar.
No abstract available

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Figures

Figure 1
Figure 1
Interactions proposed to mediate platelet adhesion and aggregation during thrombus formation. Events are depicted from left to right as they may occur in temporal sequence, initiating with platelet tethering to a reactive surface. At shear rates of less than 500–1,000 s–1, stable adhesion may occur independently of the initial vWF–GP Ibα interaction. The scheme considers only known adhesive interactions and does not exclude the relevance of other ligand-receptor pairs for platelet thrombus formation and other agonists in platelet activation. The 2 arrows connecting activation and stable adhesion express the hypothesis that activation usually precedes stable adhesion, particularly when thrombus formation occurs under the influence of high shear stress, but specific adhesive bonds may also enhance activation. (Modified from Savage et al. [10] and reprinted with permission.)
Figure 2
Figure 2
Schematic representation of the mechanisms of platelet adhesion and aggregation in flowing blood. In a cylindrical vessel, the velocity profile of particles contained in circulating blood is parabolic; the shear rate decreases from the wall to the center of the lumen inversely to the flow velocity. In a flow field with high shear rate, only GP Ibα interaction with immobilized vWF multimers can initiate the tethering of circulating platelets to the vessel wall and to already adherent platelets. This GP Ibα–dependent interaction supports initially transient bonds, depicted by the ongoing detachment of the 2 top platelets from vWF multimers bound to already activated platelets. The process is amplified by the activation of αIIbβ3, which may occur during the transient tethering or through the action of other receptors that bind collagen or other components of exposed vascular or extravascular surfaces (see also Figure 1). The final result is stable attachment of recruited platelets and irreversible membrane binding of soluble adhesive ligand (fibrinogen and vWF), thus providing the substrate for additional recruitment of nonactivated platelets and leading to thrombus growth. Note that nonactivated αIIbβ3 cannot bind soluble ligands. The bridging effect of fibrinogen, which is required to stabilize platelet aggregation and resist the effects of high shear stress, only occurs after initial tethering of platelets through the interaction of vWF and GP Ibα. At shear rates less than 500–1,000 s–1, the adhesive functions of vWF are no longer indispensable, either for initial attachment to a thrombogenic surface or for aggregation. Thus, even in the absence of vWF, collagen receptors (among others) can permit stable adhesive interactions to form rapidly, and fibrin or fibrinogen can bind to platelets to permit aggregation.
See this image and copyright information in PMC

Comment on

  • A revised model of platelet aggregation.
    Kulkarni S, Dopheide SM, Yap CL, Ravanat C, Freund M, Mangin P, Heel KA, Street A, Harper IS, Lanza F, Jackson SP. Kulkarni S, et al. J Clin Invest. 2000 Mar;105(6):783-91. doi: 10.1172/JCI7569. J Clin Invest. 2000. PMID: 10727447 Free PMC article.

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