At the initial stage of hemostasis or thrombosis, blood platelets attach to the injury and become immobilized on vascular surface. This initial platelet aggregation provides the basis for biochemical reactions, hardening of the blood clot and cessation of bleeding. Therefore, a detailed study of the first stages of adhesion and platelet aggregation is an urgent task. The mechanism of primary platelet adhesion in arterial hydrodynamic conditions is based mainly on the specific key-lock interactions between the transmembrane platelet glycoprotein GPIb and the plasma protein von Willebrand factor. The von Willebrand factor (VWF) is a multimeric plasma protein that provides platelet adhesion to injury in the arteries and microvessels. This paper presents a three-dimensional computer model that allows one to explicitly describe the dynamics, conformational changes, and activation of VWF by hydrodynamic forces. The model is based on the combination of the Boltzmann lattice method with fluctuations to simulate hydrodynamics and a coarse-grained particle dynamics model for describing the dynamics of a polymer chain in a viscous fluid. The model was verified by comparing the results of calculations with experimental data found in the literature. Numerical results show that the contour length of the multimer is an important parameter regulating the thrombogenicity of VWF in the blood. The model also showed that attachment to the surface contributes to the activation of VWF and platelet adhesion. The results can be used in a multiscale computer simulation of the growth of blood clots in blood vessels.
von Willebrand factor, thrombosis, hemostasis, hydrodynamic activation, mechano-chemical regulation, computer simulations
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