Diaz-Ricart M, Tandon N N, Gómez-Ortiz G, Carretero M, Escolar G, Ordinas A, Jamieson G A
Servicio Hemoterapia y Hemostasia, Hospital Clínic i Provincial, Barcelona, Spain.
Arterioscler Thromb Vasc Biol. 1996 Jul;16(7):883-8. doi: 10.1161/01.atv.16.7.883.
The membrane glycoprotein CD36 (glycoprotein [GP] IV) has previously been shown to accelerate the initial interaction of platelets with purified type I collagen in both static and flow systems. In the present study, the role of CD36 on platelet interaction with physiologically relevant collagenous surfaces was addressed. Using arterial subendothelium (SE) and endothelial cell extracellular matrix (ECM), studies were performed under flow conditions with annular and parallel-plate perfusion chambers, respectively, at a shear rate of 800 s-1 for 2, 5, and 10 minutes. Perfusates consisted of citrated normal blood samples incubated with Fab fragments of a monospecific polyclonal anti-CD36 antibody or with each of three new anti-CD36 monoclonal antibodies (MoAbs) that inhibit platelet adhesion to purified type I collagen in a static system (131.4, 131.5, and 131.7). Perfusions over SE were also carried out using citrated blood samples from a Naka-negative donor, whose platelets lack CD36. Morphometric evaluation of the perfused samples showed that polyclonal anti-CD36 Fab and the three monoclonal anti-CD36 antibodies inhibited platelet adhesion to the two substrates by 40% after 2 minutes of perfusion and by 30% after 5 minutes (P < .005 on SE and P < .01 on ECM), but at 10 minutes, significant inhibition was seen only on SE with polyclonal anti-CD36 Fab. Similar inhibitions were seen with Naka-negative platelets on SE. These studies demonstrate that CD36 plays a role in the early stages of platelet adhesion to physiologically relevant subendothelial surfaces.
膜糖蛋白CD36（糖蛋白[GP]IV）先前已被证明在静态和流动系统中均可加速血小板与纯化的I型胶原的初始相互作用。在本研究中，探讨了CD36在血小板与生理相关胶原表面相互作用中的作用。分别使用动脉内皮下层（SE）和内皮细胞细胞外基质（ECM），在环形和平行板灌注室的流动条件下进行研究，剪切速率为800 s-1，持续2、5和10分钟。灌注液由柠檬酸盐化的正常血液样本组成，这些样本与单特异性多克隆抗CD36抗体的Fab片段或三种新的抗CD36单克隆抗体（MoAbs）中的每一种一起孵育，这三种单克隆抗体在静态系统中可抑制血小板与纯化的I型胶原的粘附（131.4、131.5和131.7）。还使用来自Naka阴性供体的柠檬酸盐化血液样本对SE进行灌注，该供体的血小板缺乏CD36。对灌注样本的形态计量学评估表明，多克隆抗CD36 Fab和三种抗CD36单克隆抗体在灌注2分钟后可使血小板与两种底物的粘附抑制40%，在灌注5分钟后抑制30%（在SE上P <.005，在ECM上P <.01），但在10分钟时，仅在使用多克隆抗CD36 Fab的SE上观察到显著抑制。在SE上，Naka阴性血小板也观察到类似的抑制作用。这些研究表明，CD36在血小板粘附于生理相关内皮下表面的早期阶段起作用。
