Yamamoto K, Kitagawa H, Tanoue K, Tsuruo T, Yamamoto N, Yamazaki H
Thromb Haemost. 1986 Aug 20;56(1):90-4.
B16 mouse melanoma cell lines (B16F1, B16F10 and B16BL6) were able to induce platelet aggregation, and concomitant release of ATP in heparinized platelet-rich plasma (PRP). In citrated PRP, these tumor cells did not induce platelet aggregation. Addition of heparin to citrated PRP enabled these tumor cells to induce aggregation. In heparinized PRP, platelet aggregates induced by B16F10 cells were dissociated by the addition of either 4 mM EDTA, 10 mM CaCl2 or 0.1 micrograms/ml protamine sulfate. B16F10-induced aggregation in heparinized PRP was inhibited by preincubation with anti-fibronectin antibody, but not with antifibrinogen or anti-von Willebrand factor antibodies. B16F10 cells induced aggregation in washed platelet suspension with the addition of heparinized platelet-poor plasma (PPP). Cryoprecipitate from human plasma showed the same effect in the presence of heparin if substituted for PPP. The mixture of purified fibronectin, von Willebrand factor, fibrinogen and heparin were less effective than cryoprecipitate on B16F10-induced aggregation of washed platelets. The results suggest that an interaction between fibronectin and heparin may be important in tumor cell-induced aggregation.
B16小鼠黑色素瘤细胞系（B16F1、B16F10和B16BL6）能够在肝素化富血小板血浆（PRP）中诱导血小板聚集，并伴随ATP的释放。在枸橼酸化PRP中，这些肿瘤细胞不会诱导血小板聚集。向枸橼酸化PRP中添加肝素能使这些肿瘤细胞诱导聚集。在肝素化PRP中，B16F10细胞诱导的血小板聚集体可通过添加4 mM乙二胺四乙酸（EDTA）、10 mM氯化钙或0.1微克/毫升硫酸鱼精蛋白而解离。在肝素化PRP中，B16F10诱导的聚集可通过与抗纤连蛋白抗体预孵育而受到抑制，但与抗纤维蛋白原或抗血管性血友病因子抗体预孵育则无此作用。在添加肝素化乏血小板血浆（PPP）的洗涤血小板悬液中，B16F10细胞诱导聚集。如果用人血浆冷沉淀替代PPP，在肝素存在的情况下也显示出相同的效果。纯化的纤连蛋白、血管性血友病因子、纤维蛋白原和肝素的混合物对B16F10诱导的洗涤血小板聚集的作用不如冷沉淀有效。结果表明，纤连蛋白与肝素之间的相互作用在肿瘤细胞诱导的聚集中可能很重要。
