Fig. 3.
Fig. 3. Model of platelet interaction with collagen under flow conditions. The first step is the arrest of blood platelets on collagen (A + B). The interaction between GPIb-vWF and specific and high-affinity vWF-binding sites in collagen results in a marked loss of velocity of the blood platelet (A). The actual arrest of platelets occurs after α2β1-collagen interaction (B). This may also result in some degree of activation (*). Both vWF and α2β1 bind to specific adhesive sites on collagen that are depicted as solid rectangles. The second step is the binding of other collagen receptors (Col-R; eg, GP VI) to simple collagen sequences (delineating the collagen triple helix) that are depicted as open rectangles. This results in full platelet activation (**), firm attachment, and GPIIb/IIIa activation.

Model of platelet interaction with collagen under flow conditions. The first step is the arrest of blood platelets on collagen (A + B). The interaction between GPIb-vWF and specific and high-affinity vWF-binding sites in collagen results in a marked loss of velocity of the blood platelet (A). The actual arrest of platelets occurs after α2β1-collagen interaction (B). This may also result in some degree of activation (*). Both vWF and α2β1 bind to specific adhesive sites on collagen that are depicted as solid rectangles. The second step is the binding of other collagen receptors (Col-R; eg, GP VI) to simple collagen sequences (delineating the collagen triple helix) that are depicted as open rectangles. This results in full platelet activation (**), firm attachment, and GPIIb/IIIa activation.

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