Antibodies to CD36 (GPIV) inhibit platelet adhesion to subendothelial surfaces under flow conditions.
Antibodies to CD36 (GPIV) inhibit platelet adhesion to subendothelial surfaces under flow conditions.
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CD36 (GPIV) 抗体在流动条件下抑制血小板粘附至内皮下表面。
DOI：
10.1161/01.atv.16.7.883
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Jamieson,GA
中科院分区：
文献类型：
--
作者：
Diaz-Ricart,M;Tandon,NN;Gómez-Ortiz,G;Carretero,M;Escolar,G;Ordinas,A;Jamieson,GA
膜糖蛋白CD 36（糖蛋白[GP] IV）先前已被证明在静态和流动系统中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，CD 36对血小板与生理相关的胶原表面相互作用的作用得到解决。使用动脉内皮下（SE）和内皮细胞细胞外基质（ECM），分别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。灌注液由柠檬酸盐处理的正常血液样本组成，这些样本与单特异性多克隆抗CD 36抗体的Fab片段或与三种新型抗CD 36单克隆抗体（MoAb）中的每一种孵育，这些抗体在静态系统中抑制血小板与纯化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血液样本进行SE灌注，该供体的血小板缺乏CD 36。灌注样品的形态学评估显示，多克隆抗CD 36 Fab和三种单克隆抗CD 36抗体在灌注2分钟后抑制血小板与两种基质的粘附40%，5分钟后抑制30%（SE上P<0.005，ECM上P <0.01），但在10分钟时，仅在SE上观察到多克隆抗CD 36 Fab的显著抑制。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，CD 36在血小板粘附到生理相关的内皮下表面的早期阶段起作用。
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−1for 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 andP<.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.