Theret N, Delbart C, Aguie G, Fruchart J C, Vassaux G, Ailhaud G
SERLIA, U325 INSERM, Institut Pasteur, Lille, France.
Biochem Biophys Res Commun. 1990 Dec 31;173(3):1361-8. doi: 10.1016/s0006-291x(05)80938-6.
Apolipoprotein A-I (apo A-I)*/DMPC complexes have been previously shown to promote cholesterol efflux from cholesterol-preloaded adipose cells whereas apo A-II/DMPC complexes, which bind to the same cell surface binding sites, were ineffective. Addition of apo A-I/DMPC complexes led to a rapid and transient formation of diacylglycerol. However, in contrast to PGF2 alpha (Doglio et al., Proc. Natl. Acad. Sci. USA, 1989, 86, 1148), no accumulation of inositol phosphates was observed. Apo A-II/DMPC complexes had no effect on diacylglycerol formation. Stimulation by apo A-I/DMPC complexes or native HDL3 of cells prelabelled with (2-palmitoyl 9,10[3H])phosphatidylcholine induced also the formation of labelled diacylglycerol whereas apo A-II/DMPC complexes and HDL3 treated with tetranitromethane showed no effect. Direct activation of protein kinase C(s) by PMA promoted cholesterol efflux providing that DMPC liposomes were present as cholesterol acceptor. It is proposed that lipoprotein particles have two separate effects, i.e. a ligand-induced effect leading to cholesterol translocation from intracellular stores to the cell surface and a bilayer-induced effect allowing cholesterol efflux from the cell surface to the acceptor.
载脂蛋白A-I（apo A-I）*/二肉豆蔻酰磷脂酰胆碱（DMPC）复合物先前已被证明可促进胆固醇从预先加载胆固醇的脂肪细胞中流出，而结合到相同细胞表面结合位点的载脂蛋白A-II/DMPC复合物则无效。添加apo A-I/DMPC复合物会导致二酰基甘油快速短暂形成。然而，与前列腺素F2α（Doglio等人，《美国国家科学院院刊》，1989年，86卷，1148页）不同，未观察到肌醇磷酸的积累。载脂蛋白A-II/DMPC复合物对二酰基甘油的形成没有影响。用（2-棕榈酰9,10[3H]）磷脂酰胆碱预标记的细胞，经apo A-I/DMPC复合物或天然HDL3刺激也会诱导标记的二酰基甘油形成，而载脂蛋白A-II/DMPC复合物和用四硝基甲烷处理的HDL3则无此作用。如果存在DMPC脂质体作为胆固醇受体，佛波酯（PMA）直接激活蛋白激酶C可促进胆固醇流出。有人提出脂蛋白颗粒有两种独立的作用，即配体诱导的作用导致胆固醇从细胞内储存部位转运到细胞表面，以及双层诱导的作用使胆固醇从细胞表面流出到受体。
