Dunn R C, Schachter M, Miles C M, Feher M D, Tranter P R, Bruckdorfer K R, Sever P S
Department of Biochemistry, Royal Free Hospital School of Medicine, London, England.
FEBS Lett. 1988 Oct 10;238(2):357-60. doi: 10.1016/0014-5793(88)80512-x.
Low-density lipoproteins activate isolated human platelets. The mechanism of this activation is unknown, but may involve increased phosphoinositide turnover. We have examined the effect of low-density lipoproteins on intracellular calcium concentrations in platelets loaded with the photoprotein aequorin. The lipoproteins induced concentration-dependent increases in intracellular calcium, associated with shape change and aggregation. These responses could be partially inhibited by the removal of extracellular calcium and by pre-incubation with acetylsalicylic acid. They were also antagonised by agents which increase cellular concentrations of cyclic adenosine and guanosine monophosphates. It is not clear whether the platelet-lipoprotein interaction involves a 'classical' lipoprotein receptor.
低密度脂蛋白可激活分离出的人体血小板。这种激活机制尚不清楚,但可能涉及磷酸肌醇代谢增加。我们研究了低密度脂蛋白对装载发光蛋白水母发光蛋白的血小板细胞内钙浓度的影响。这些脂蛋白可引起细胞内钙浓度呈浓度依赖性增加,并伴有形态变化和聚集。去除细胞外钙以及用乙酰水杨酸预孵育可部分抑制这些反应。它们也受到增加细胞内环磷酸腺苷和环磷酸鸟苷浓度的试剂的拮抗。目前尚不清楚血小板与脂蛋白的相互作用是否涉及“经典”的脂蛋白受体。