Adachi I, Takahashi M, Adachi H, Horikoshi I
Cell Struct Funct. 1986 Jun;11(2):157-63. doi: 10.1247/csf.11.157.
EL-4 tumor cells were assayed in vitro for their ability to aggregate two kinds of platelets. An inhibition study showed that the EL-4 tumor cell can induce platelet aggregation by at least two different mechanisms. One, mediated by thrombin, was dominant with rabbit platelets because hirudin, which specifically inhibits thrombin, considerably suppressed the rabbit platelet aggregation induced by EL-4 tumor cells. In contrast, EL-4 cells induced the aggregation of human platelets even in citrated PRP. It is the apyrase-sensitive pathway that is believed to work in human platelets. The human platelet responses to EL-4 tumor cells clearly differed from those of rabbit platelets in terms of inhibition by hirudin and apyrase and of reactivity in citrated PRP. Both phospholipase A2 and dibutyryl cAMP strongly inhibited EL-4 tumor cell-induced platelet aggregation in both rabbit and human platelets. These two compounds may block a vital step in platelet aggregation that is elicited by the EL-4 tumor cells. Our results show that human platelet response to tumor cells is not necessarily deducible from experimental data obtained with animal platelets.
对EL-4肿瘤细胞进行体外测定，以评估其使两种血小板聚集的能力。一项抑制研究表明，EL-4肿瘤细胞可通过至少两种不同机制诱导血小板聚集。一种由凝血酶介导，对兔血小板起主要作用，因为特异性抑制凝血酶的水蛭素可显著抑制EL-4肿瘤细胞诱导的兔血小板聚集。相比之下，即使在枸橼酸化富血小板血浆（PRP）中，EL-4细胞也能诱导人血小板聚集。据信在人血小板中起作用的是对腺苷三磷酸双磷酸酶敏感的途径。就水蛭素和腺苷三磷酸双磷酸酶的抑制作用以及在枸橼酸化PRP中的反应性而言，人血小板对EL-4肿瘤细胞的反应明显不同于兔血小板。磷脂酶A2和二丁酰环磷腺苷均强烈抑制EL-4肿瘤细胞诱导的兔和人血小板聚集。这两种化合物可能会阻断EL-4肿瘤细胞引发的血小板聚集中的关键步骤。我们的结果表明，人血小板对肿瘤细胞的反应不一定能从动物血小板的实验数据中推导出来。
