Couderc R, Bonneau C, Tissot M, Bailleul S, Roch-Arveiller M, Giroud J P
Laboratoire de Biochimie, Hôpital Tenon, Paris, France.
Biofactors. 1997;6(2):157-63. doi: 10.1002/biof.5520060209.
Polymorphonuclear leukocytes (PMN) generate highly reactive oxygen derived free radicals that may cause lipoprotein lipid oxidation and so contribute to the pathogenesis of atherosclerosis. On the other hand it has been shown that lipoproteins can alter cell functions in vitro. We therefore studied the effects of atherogenic lipoproteins, VLDL and LDL, on the production of superoxide anion by human PMN in the presence or absence of formyl-methionyl-leucyl-phenylalanine (fMLP). VLDL and LDL stimulate PMN superoxide production and potentialize PMN stimulation by fMLP. The lipid moiety of the lipoproteins might be mainly involved in these effects. The binding of radio-labelled fMLP to its specific membrane receptor was significantly enhanced in the presence of VLDL and only slightly in the presence of LDL. The study of the signal transduction suggests that modulation of phospholipase D and A2 activities could be involved in the modification by LDL of PMN response to fMLP.
多形核白细胞（PMN）会产生高反应性的氧衍生自由基，这些自由基可能导致脂蛋白脂质氧化，从而促进动脉粥样硬化的发病机制。另一方面，研究表明脂蛋白可在体外改变细胞功能。因此，我们研究了致动脉粥样硬化脂蛋白极低密度脂蛋白（VLDL）和低密度脂蛋白（LDL）在存在或不存在甲酰甲硫氨酰亮氨酰苯丙氨酸（fMLP）的情况下对人PMN产生超氧阴离子的影响。VLDL和LDL刺激PMN产生超氧阴离子，并增强fMLP对PMN的刺激作用。脂蛋白的脂质部分可能主要参与这些作用。在VLDL存在的情况下，放射性标记的fMLP与其特异性膜受体的结合显著增强，而在LDL存在的情况下仅略有增强。信号转导研究表明，磷脂酶D和A2活性的调节可能参与LDL对PMN对fMLP反应的修饰。
