Aihara M, Tamura K, Kawarada R, Okawa K, Yoshida Y
First Department of Internal Medicine, Hirosaki University School of Medicine, Japan.
Thromb Haemost. 1988 Oct 31;60(2):182-7.
The adhesion of human fixed washed platelets (FWP) to collagen was decreased after treatment with Serratia marcescens protease (SP), which removed 95% of the glycocalicin from platelet membrane glycoprotein (GP) Ib. However, the diminished adhesion of SP treated FWP to collagen could still be increased in the presence of purified von Willebrand factor (vWF). This ability to vWF to increase FWP adhesion to collagen is defined as collagen cofactor (CCo). The adhesion of FWP to collagen was not affected by a monoclonal antibody (MAb) to GP IIb/IIIa (10E5), that inhibits ADP and collagen induced platelet aggregation. On the other hand, it was decreased by 50% by a MAb to GP Ib (6D1), that inhibits ristocetin induced platelet aggregation. Adhesion of FWP in buffer to collagen was completely inhibited by Ricinus communis agglutinin I or concanavalin A, while Lens culinalis agglutinin and wheat germ agglutinin showed 50% inhibition. The FWP adhesion to collagen in the presence of vWF (normal plasma) was unaffected by MAbs to GP IIb/IIIa (10E5, P2, HPL1) but was decreased to 32-38% by MAbs to GP Ib (6D1, AN51, HPL11). A MAb to vWF (CLB-RAg 35), that inhibits ristocetin induced binding of vWF to platelets, decreased the CCo of normal plasma by 70%. The MAb, CLB-RAg 201, that inhibits the binding of vWF to collagen, completely inhibited the CCo of normal plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
用粘质沙雷氏菌蛋白酶（SP）处理后，人固定洗涤血小板（FWP）与胶原蛋白的黏附力降低，该蛋白酶从血小板膜糖蛋白（GP）Ib上去除了95%的糖萼蛋白。然而，在存在纯化的血管性血友病因子（vWF）的情况下，经SP处理的FWP与胶原蛋白黏附力的降低仍可得到增强。vWF增强FWP与胶原蛋白黏附的这种能力被定义为胶原蛋白辅因子（CCo）。FWP与胶原蛋白的黏附不受针对GP IIb/IIIa的单克隆抗体（MAb，10E5）的影响，该抗体抑制ADP和胶原蛋白诱导的血小板聚集。另一方面，针对GP Ib的MAb（6D1）使其降低了50%，该抗体抑制瑞斯托菌素诱导的血小板聚集。蓖麻凝集素I或伴刀豆球蛋白A可完全抑制缓冲液中FWP与胶原蛋白的黏附，而菜豆凝集素和麦胚凝集素则显示出50%的抑制作用。在vWF（正常血浆）存在的情况下，FWP与胶原蛋白的黏附不受针对GP IIb/IIIa的MAb（10E5、P2、HPL1）的影响，但针对GP Ib的MAb（6D1、AN51、HPL11）可使其降低至32 - 38%。一种抑制瑞斯托菌素诱导的vWF与血小板结合的针对vWF的MAb（CLB - RAg 35）使正常血浆的CCo降低了70%。抑制vWF与胶原蛋白结合的MAb CLB - RAg 201完全抑制了正常血浆的CCo。（摘要截短于250字）
