Blood group alters platelet binding kinetics to von Willebrand factor and consequently platelet function

Author:

Dunne Eimear1ORCID,Qi Qin M.2ORCID,Shaqfeh Eric S.2,O’Sullivan Jamie M.1,Schoen Ingmar1ORCID,Ricco Antonio J.3ORCID,O’Donnell James S.1ORCID,Kenny Dermot1ORCID

Affiliation:

1. Irish Centre for Vascular Biology and Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland; and

2. Department of Chemical Engineering and

3. Department of Electrical Engineering, Stanford University, Stanford, CA

Abstract

Abstract Blood type O is associated with a lower risk of myocardial infarction. Platelets play a critical role in myocardial infarction. It is not known whether the expression of blood group antigens on platelet proteins alters platelet function; we hypothesized that platelet function would be different between donors with blood type O and those with non-O. To address this hypothesis, we perfused blood from healthy type O donors (n = 33) or non-O donors (n = 54) over pooled plasma derived von Willebrand factor (VWF) protein and purified blood type–specific VWF at arterial shear and measured platelet translocation dynamics. We demonstrate for the first time that type O platelets travel farther at greater speeds before forming stable bonds with VWF. To further characterize these findings, we used a novel analytical model of platelet interaction. Modeling revealed that the kinetics for GPIb/VWF binding rate are significantly lower for type O compared with non-O platelets. Our results demonstrate that platelets from type O donors interact less with VWF at arterial shear than non-O platelets. Our results suggest a potential mechanism for the reduced risk of myocardial infarction associated with blood type O.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference38 articles.

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