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Macromolecules That Link Platelets following Vessel Wall Injury a
Author(s) -
HAWIGER JACEK
Publication year - 1987
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1987.tb30990.x
Subject(s) - platelet , receptor , chemistry , von willebrand factor , platelet membrane glycoprotein , fibrinogen , glycoprotein , glycoprotein ib , microbiology and biotechnology , biophysics , platelet activation , macromolecule , platelet adhesiveness , cell surface receptor , biochemistry , platelet aggregation , biology , immunology
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.