Tomita Aiko, Tamura Noriko, Nanazawa Yohei, Shiozaki Seiji, Goto Shinya
Department of Medicine (Cardiology), Tokai University School of Medicine.
J Atheroscler Thromb. 2015;22(2):201-10. doi: 10.5551/jat.26203. Epub 2014 Oct 6.
Computer simulation is a new method for understanding biological phenomena. In this report, we developed a simple platelet simulator representing platelet adhesion under blood flow conditions.
We generated virtual platelets based on the functions of three key adhesive proteins: glycoprotein (GP) Ibα, GPIIb/IIIa and collagen receptors. The adhesive force between GPIbα and von Willebrand factor (VWF) was set to increase in association with increments in the fluid shear stress. GPIIb/IIIa acquires an adhesive force to bind with ligands only when platelets are activated following multiple GPIbα stimulation by VWF or collagen receptors.
Upon perfusion over the area of virtual endothelial injury, the virtual platelets adhered and became activated to form platelet thrombi. A total of 286/mm(2) of activated platelets was found to have accumulated downstream of the flow obstacle within 30 seconds, with 59/mm(2) platelets adhering upstream. The results obtained with the virtual model were consistent with those for real platelets in human blood in the presence of similarly shaped flow obstacles.
Our computer platelet simulator, which employs the functions of three key platelet membrane proteins, shows similar findings for adhesion in the presence and absence of blood flow obstacles.
计算机模拟是一种理解生物现象的新方法。在本报告中,我们开发了一种简单的血小板模拟器,用于模拟血流条件下的血小板黏附。
我们基于三种关键黏附蛋白的功能生成虚拟血小板:糖蛋白(GP)Ibα、GPIIb/IIIa和胶原受体。GPIbα与血管性血友病因子(VWF)之间的黏附力设定为随流体剪切应力的增加而增加。只有当血小板在VWF或胶原受体多次刺激GPIbα后被激活时,GPIIb/IIIa才获得与配体结合的黏附力。
在虚拟内皮损伤区域进行灌注时,虚拟血小板黏附并被激活形成血小板血栓。发现在30秒内,共有286个/mm²的激活血小板积聚在流动障碍物下游,59个/mm²的血小板黏附在上游。在存在类似形状的流动障碍物的情况下,虚拟模型获得的结果与人体血液中真实血小板的结果一致。
我们的计算机血小板模拟器利用三种关键血小板膜蛋白的功能,在有无血流障碍物的情况下均显示出相似的黏附结果。