About: Platelet Aggregation Process is a research topic. Over the lifetime, 25 publications have been published within this topic receiving 2040 citations.
TL;DR: An important role for platelet vWf in initiating the platelet aggregation process under flow is demonstrated and the currently accepted view that the vWF-GPIbalpha interaction is exclusively involved in initiating platelet aggregating at elevated shear rates is challenged.
Abstract: In this study we have examined the mechanism of platelet aggregation under physiological flow conditions using an in vitro flow-based platelet aggregation assay and an in vivo rat thrombosis model. Our studies demonstrate an unexpected complexity to the platelet aggregation process in which platelets in flowing blood continuously tether, translocate, and/or detach from the luminal surface of a growing platelet thrombus at both arterial and venous shear rates. Studies of platelets congenitally deficient in von Willebrand factor (vWf) or integrin αIIbβ3 demonstrated a key role for platelet vWf in mediating platelet tethering and translocation, whereas integrin αIIbβ3 mediated cell arrest. Platelet aggregation under flow appears to be a multistep process involving: (a) exposure of vWf on the surface of immobilized platelets; (b) a reversible phase of platelet aggregation mediated by the binding of GPIbα on the surface of free-flowing platelets to vWf on the surface of immobilized platelets; and (c) an irreversible phase of aggregation dependent on integrin αIIbβ3. Studies of platelet thrombus formation in vivo demonstrate that this multistep adhesion mechanism is indispensable for platelet aggregation in arterioles and also appears to promote platelet aggregate formation in venules. Together, our studies demonstrate an important role for platelet vWf in initiating the platelet aggregation process under flow and challenge the currently accepted view that the vWf-GPIbα interaction is exclusively involved in initiating platelet aggregation at elevated shear rates.
TL;DR: A new mechanism initiating platelet aggregation that is critically influenced by shear, physical proximity between translocating platelets, and membrane tether formation is identified and a model to explain how the discoid morphology of platelets facilitates the maintenance of adhesive interactions with thrombogenic surfaces under high shear stress conditions is provided.
TL;DR: The hypothesis that the interaction of fibrinogen with thrombospondin on the activated platelet surface may be an important step in the platelet aggregation process is supported.
Abstract: Using an enzyme-linked immunosorbent assay, we have demonstrated that purified human fibrinogen forms a complex with adsorbed platelet thrombospondin. The formation of the fibrinogen-thrombospondin complex was specific, saturable, and partially inhibited by mannosamine, glucosamine, and arginine. These same inhibitors have been previously shown to block thrombin-induced platelet lectin activity and platelet thrombospondin lectin activity. Adsorbed thrombospondin also formed a complex with fibronectin, although the extent of complex formation was significantly less than the extent of formation of the fibrinogen-thrombospondin complex. Platelet membrane glycoproteins IIb and IIIa, which have been previously shown to bind fibrinogen, did not inhibit the formation of the fibrinogen-thrombospondin complex. The present study supports the hypothesis that the interaction of fibrinogen with thrombospondin on the activated platelet surface may be an important step in the platelet aggregation process.
TL;DR: Glycoprotein IIIb, by interacting with thrombospondin on the activated platelet surface, may play an important role in the platelet aggregation process.
TL;DR: This work aims to demonstrate the importance of knowing the carrier and removal status of canine coronavirus, as a source of infection for other animals, not necessarily belonging to the same breeds.