Adhesive functions of platelets lacking glycoprotein IV (CD36).
Adhesive functions of platelets lacking glycoprotein IV (CD36).
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DOI：
10.1182/blood.v78.11.2809.bloodjournal78112809
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发表时间：
1991
期刊：
影响因子：
20.3
通讯作者：
N. Tandon;C. Ockenhouse;N. Greco;G. Jamieson
中科院分区：
文献类型：
--
作者：
N. Tandon;C. Ockenhouse;N. Greco;G. Jamieson
糖蛋白IV（GPIV; CD 36或GPIIb）是一种细胞表面糖蛋白，已提出其介导许多生理学上重要的过程，如血小板与血小板反应蛋白（TSP）和胶原的粘附、恶性疟原虫感染的红细胞的细胞粘附以及单核细胞与血小板和巨噬细胞的TSP依赖性相互作用。由于Naka阴性表型的血小板最近被证明缺乏可检测的GPIV，它们的可用性提供了直接测试这些关于其粘附功能的假设的机会。已发现Naka阴性血小板和单核细胞不支持恶性疟原虫感染的红细胞的细胞粘附。Naka阴性血小板在其与纤维状胶原的粘附的初始阶段是缺乏的，并且这种缺陷在无Mg（2+）条件下最显著。最后，与正常对照组相比，Naka阴性血小板在活化前后结合TSP的能力未受损。这些结果不支持GPIV作为TSP受体的作用。
Glycoprotein IV (GPIV; CD36 or GPIIIb) is a cell surface glycoprotein that has been proposed as mediating a number of physiologically important processes such as the adhesion of platelets to thrombospondin (TSP) and collagen, the cytoadherence of Plasmodium falciparum-infected erythrocytes, and the TSP-dependent interaction of monocytes with platelets and macrophages. Because platelets of the Naka-negative phenotype have recently been shown to lack detectable GPIV, their availability offered the opportunity to test directly these hypotheses regarding its adhesive functions. It has been found that Naka-negative platelets and monocytes do not support cytoadherence of P falciparum-infected erythrocytes. Naka-negative platelets are deficient in the initial stages of their adhesion to fibrillar collagen and this defect is most marked under Mg(2+)-free conditions. Finally, the ability of Naka-negative platelets to bind TSP before or after activation is unimpaired as compared with normal controls. These results do not support a role for GPIV as the TSP receptor.