Knorr M, Locher R, Vogt E, Vetter W, Block L H, Ferracin F, Lefkovits H, Pletscher A
Department of Medicine, University of Zürich, Switzerland.
Eur J Biochem. 1988 Mar 15;172(3):753-9. doi: 10.1111/j.1432-1033.1988.tb13953.x.
The interaction of low-density lipoprotein (LDL) with the human platelet was investigated with regard to saturable high-affinity binding, shape change, cytosolic free Ca2+ concentration, phosphatidylinositol (PtdIns) turnover, and thromboxane B2 biosynthesis. The experiments show that LDL, at a concentration approximately 100 times lower than in plasma, causes platelet activation concomitantly with stimulation of the PtdIns cycle and thromboxane B2 formation, similarly to other activators of platelets. The effects of LDL were inhibited by high-density lipoprotein. The results suggest that activation of platelets by low concentrations of LDL may play a role in pathophysiological conditions and that platelet can serve as a model for studying the influence of LDL on various target cells.
就可饱和的高亲和力结合、形状变化、胞质游离钙离子浓度、磷脂酰肌醇（PtdIns）周转以及血栓素B2生物合成方面，对低密度脂蛋白（LDL）与人血小板的相互作用进行了研究。实验表明，LDL浓度比血浆中浓度低约100倍时，与其他血小板激活剂类似，会伴随着磷脂酰肌醇循环和血栓素B2形成的刺激而导致血小板激活。LDL的作用被高密度脂蛋白抑制。结果表明，低浓度LDL激活血小板可能在病理生理状况中起作用，并且血小板可作为研究LDL对各种靶细胞影响的模型。
