Esumi N, Todo S, Imashuku S
Cancer Res. 1987 Apr 15;47(8):2129-35.
Platelet aggregating activity of the NCG human neuroblastoma cell line was compared with that of the HL-60 human promyelocytic leukemia cell line. NCG, in intact cell suspensions and ultracentrifuged pellets, induced platelet aggregation most significantly in heparinized platelet rich plasma (PRP) containing 2.5 units/ml of heparin, but not in the presence of higher concentrations of heparin or 5 mM ethylenediamine-tetraacetate or in citrated PRP. NCG induced platelet aggregation was also inhibited by hirudin or (2R,4R)-4-methyl-1-[N2-(3-methyl-1,2,3,4-tetrahydro-8-quinolinesulfon yl)-L- arginyl]-2-piperidinecarboxylic acid (MD 805) in the same manner as that of tissue thromboplastin induced platelet aggregation. HL-60 cells did not induce platelet aggregation in our heparinized PRP assay systems; however, after treatment with neuraminidase HL-60 cells became active in aggregating platelets in either heparinized or citrated PRP. NCG demonstrated high procoagulant activity by either intact cell suspensions or ultracentrifuged pellets. The procoagulant activity of NCG was reduced in Factor VII deficient human plasma as it was in the results obtained by tissue thromboplastin. These results suggest that NCG induces platelet aggregation via thrombin generated through procoagulant activity which is shed in association with microvesicles demonstrated in the ultracentrifuged pellets. This type of platelet aggregating activity found in NCG is significantly different from that of HL-60.
将NCG人神经母细胞瘤细胞系的血小板聚集活性与HL-60人早幼粒细胞白血病细胞系的血小板聚集活性进行了比较。在完整细胞悬液和超速离心沉淀中，NCG在含有2.5单位/毫升肝素的肝素化富血小板血浆（PRP）中诱导血小板聚集最为显著，但在更高浓度肝素、5 mM乙二胺四乙酸存在时或枸橼酸化PRP中则不会。水蛭素或(2R,4R)-4-甲基-1-[N2-(3-甲基-1,2,3,4-四氢-8-喹啉磺酰基)-L-精氨酰]-2-哌啶羧酸（MD 805）对NCG诱导的血小板聚集的抑制方式与组织凝血活酶诱导的血小板聚集相同。在我们的肝素化PRP检测系统中，HL-60细胞不会诱导血小板聚集；然而，用神经氨酸酶处理后，HL-60细胞在肝素化或枸橼酸化PRP中均能使血小板聚集。完整细胞悬液或超速离心沉淀的NCG均表现出高促凝活性。在因子VII缺乏的人血浆中，NCG的促凝活性降低，如同组织凝血活酶的结果一样。这些结果表明，NCG通过促凝活性产生的凝血酶诱导血小板聚集，促凝活性与超速离心沉淀中显示的微泡相关。在NCG中发现的这种血小板聚集活性与HL-60的显著不同。
