Macromolecules that link platelets following vessel wall injury.
Adhesive molecules are essential for anchoring platelets to the zone of vascular injury and for linking them together. Among adhesive molecules, von Willebrand factor and fibrinogen bind to platelets "on demand" when their membrane receptors, composed of membrane glycoproteins, are transformed into the binding mode. At least one receptor mechanism for fibrinogen and for vWF is controlled by ADP that is secreted through the known pathways of platelet activation and counterbalanced by cyclic AMP. Structural and functional studies of adhesive macromolecules led to delineation of receptor pathways responsible for the interaction of platelets with the injured vessel wall and with each other. Synthetic peptide analogues of platelet receptor recognition domains evolved from these studies as a new class of inhibitors of platelet aggregation.
Hawiger
J
J
Department of Medicine, New England Deaconess Hospital, Boston, Massachusetts 02215.
D000244:Adenosine Diphosphate / Q000502:physiology; D001792:Blood Platelets / Q000378:metabolism / Q000502:physiology*; D001808:Blood Vessels / Q000502:physiology*; D000242:Cyclic AMP / Q000502:physiology; D005340:Fibrinogen / Q000502:physiology; D006801:Humans; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation; D010980:Platelet Membrane Glycoproteins / Q000378:metabolism; D014841:von Willebrand Factor / Q000502:physiology
D010980:Platelet Membrane Glycoproteins; D014841:von Willebrand Factor; D000244:Adenosine Diphosphate; D005340:Fibrinogen; D000242:Cyclic AMP