Languin-Cattoën Olivier, Laborie Emeline, Yurkova Daria O, Melchionna Simone, Derreumaux Philippe, Belyaev Aleksey V, Sterpone Fabio
Laboratoire de Biochimie Théorique, CNRS, Université de Paris, UPR 9080, 13 rue Pierre et Marie Curie, F-75005 Paris, France.
Faculty of Physics, Lomonosov Moscow State University, 119991 Moscow, Russia.
Polymers (Basel). 2021 Nov 12;13(22):3912. doi: 10.3390/polym13223912.
Von Willebrand Factor (vWf) is a giant multimeric extracellular blood plasma involved in hemostasis. In this work we present multi-scale simulations of its three-domains fragment A1A2A3. These three domains are essential for the functional regulation of vWf. Namely the A2 domain hosts the site where the protease ADAMTS13 cleavages the multimeric vWf allowing for its length control that prevents thrombotic conditions. The exposure of the cleavage site follows the elongation/unfolding of the domain that is caused by an increased shear stress in blood. By deploying Lattice Boltzmann molecular dynamics simulations based on the OPEP coarse-grained model for proteins, we investigated at molecular level the unfolding of the A2 domain under the action of a perturbing shear flow. We described the structural steps of this unfolding that mainly concerns the β-strand structures of the domain, and we compared the process occurring under shear with that produced by the action of a directional pulling force, a typical condition of single molecule experiments. We observe, that under the action of shear flow, the competition among the elongational and rotational components of the fluid field leads to a complex behaviour of the domain, where elongated structures can be followed by partially collapsed melted globule structures with a very different degree of exposure of the cleavage site. Our simulations pose the base for the development of a multi-scale in-silico description of vWf dynamics and functionality in physiological conditions, including high resolution details for molecular relevant events, e.g., the binding to platelets and collagen during coagulation or thrombosis.
血管性血友病因子(vWf)是一种参与止血的巨大多聚体细胞外血浆蛋白。在这项工作中,我们展示了其三个结构域片段A1A2A3的多尺度模拟。这三个结构域对于vWf的功能调节至关重要。具体而言,A2结构域包含蛋白酶ADAMTS13切割多聚体vWf的位点,从而实现其长度控制,防止血栓形成。切割位点的暴露是由血液中剪切应力增加导致该结构域的伸长/展开引起的。通过基于蛋白质的OPEP粗粒化模型进行格子玻尔兹曼分子动力学模拟,我们在分子水平上研究了在扰动剪切流作用下A2结构域的展开。我们描述了这种展开的结构步骤,主要涉及该结构域的β链结构,并将剪切作用下发生的过程与定向拉力作用下产生的过程进行了比较,定向拉力是单分子实验的典型条件。我们观察到,在剪切流作用下,流场的伸长和旋转分量之间的竞争导致该结构域表现出复杂的行为,其中伸长结构之后可能会出现部分塌陷的熔球结构,且切割位点的暴露程度差异很大。我们的模拟为在生理条件下对vWf动力学和功能进行多尺度计算机模拟描述奠定了基础,包括分子相关事件的高分辨率细节,例如在凝血或血栓形成过程中与血小板和胶原蛋白的结合。