PLATELET-ADHESION AND AGGREGATION ON HUMAN TYPE-VI COLLAGEN SURFACES UNDER PHYSIOLOGICAL FLOW CONDITIONS

Type VI collagen is a subendothelial constituent that binds von Willeb rand factor (vWF) and platelets. The interaction of platelets with typ e VI collagen and the roles of platelet glycoprotein (GP) receptors an d vWF were studied under flow conditions using epi-fluorescent videomi croscopy coupled with digital image processing. We found that surface coverage was less than 6% on collagen VI at a relatively high-wall she ar rate (1,000 s(-1)) and was approximately 60% at a low-wall shear ra te (100 s(-1)). The molecular mechanisms involved in low-shear platele t binding were studied using monoclonal antibodies to platelet GPIb an d GPIIb-IIIa, and polymeric aurin tricarboxylic acid. Anti-GPIIb-IIIa was the most effective in eliminating adhesion (surface coverage, 0.8% ), followed by anti-GPIb (4.3%), and ATA (12.6%). Experiments with von Willebrand disease blood indicate that VWF is involved in platelet ad hesion to collagen VI at 100 s(-1). In the absence of vWF, there may b e direct binding of platelet GPIIb-IIIa complexes to collagen VI. Adhe sion and aggregation on collagen VI are different in shear rate depend ence from collagen I. Our results suggest a possible role for collagen VI and VWF in platelet adhesion and aggregation in vascular regions w ith low shear rates. (C) 1995 by The American Society of Hematology.