低密度脂蛋白激活人血小板的细胞内机制
Intracellular mechanisms in the activation of human platelets by low-density lipoproteins.
作者信息
Andrews H E, Aitken J W, Hassall D G, Skinner V O, Bruckdorfer K R
出版信息
Biochem J. 1987 Mar 1;242(2):559-64. doi: 10.1042/bj2420559.
Abstract
Low-density lipoproteins (LDL) have been shown to cause aggregation of human blood platelets at concentrations above 2 g of protein/l. The secretion of the contents of platelet dense granules was detected, but not that of the lysosomes. LDL gave rise to a mobilization of [3H]arachidonic acid from phospholipids and the appearance of products of the cyclo-oxygenase pathway after only 10 s. LDL-promoted aggregation was inhibited by both aspirin and indomethacin. There was an increase in 3H-labelled diacylglycerols and the phosphorylation of 47 kDa proteins. LDL therefore shares at least some of the mechanisms of stimulus/response coupling with those of other agonists.
摘要
低密度脂蛋白（LDL）已被证明，当蛋白质浓度高于2克/升时会导致人血小板聚集。检测到血小板致密颗粒内容物的分泌，但未检测到溶酶体内容物的分泌。LDL仅在10秒后就导致了[3H]花生四烯酸从磷脂中的动员以及环氧化酶途径产物的出现。阿司匹林和吲哚美辛均抑制LDL促进的聚集。3H标记的二酰甘油增加，47 kDa蛋白发生磷酸化。因此，LDL与其他激动剂至少共享一些刺激/反应偶联机制。
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