Abstract Programmed cell death of non-nucleated blood cells – platelets – could be associated with pathophysiology of oncologic and oncohematologic diseases. It contributes to both bleedings (caused by the thrombocytopenia, which is induced by elimination of the platelets) and thrombosis (caused by the processes of blood coagulation on the surface of phosphatidylserine exposing platelets). Here we characterized functional responses of platelets from the patients with various oncological disorders undergoing chemotherapy and compared them to the platelets from the healthy donors and platelets pre-incubated with apoptosis inducer ABT-737. Some patients exhibited diminished capability of platelets to aggregate. Immunophenotyping of these platelets revealed their pre-activation in comparison to the platelets from the healthy donors. Calcium signaling analysis revealed that in the patient-derived platelets, as well as in the apoptotic platelets, intracellular calcium levels were increased in resting cells. However, moderate level of this increase together with weak expression of phosphatidylserine allows us to assume that apoptotic processes in the circulating platelets from the patients are limited.

中文翻译：

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血液系统疾病中血小板的程序性细胞死亡和功能活性

摘要 无核血细胞——血小板——的程序性细胞死亡可能与肿瘤和血液系统疾病的病理生理学有关。它会导致出血（由血小板减少引起的血小板减少症引起）和血栓形成（由暴露血小板的磷脂酰丝氨酸表面的凝血过程引起）。在这里，我们表征了来自接受化疗的各种肿瘤疾病患者的血小板的功能反应，并将它们与来自健康供体的血小板和用凋亡诱导剂 ABT-737 预孵育的血小板进行比较。一些患者表现出血小板聚集能力减弱。与来自健康供体的血小板相比，这些血小板的免疫表型揭示了它们的预活化。钙信号分析显示，在患者来源的血小板以及凋亡血小板中，静息细胞中的细胞内钙水平增加。然而，这种增加的中等水平以及磷脂酰丝氨酸的微弱表达使我们能够假设患者循环血小板中的细胞凋亡过程是有限的。