Desrumaux C, Athias A, Masson D, Gambert P, Lallemant C, Lagrost L
Laboratoire de Biochimie des Lipoprotéines, INSERM CJF 93-10, Faculté de Médecine, Dijon, France.
J Lipid Res. 1998 Jan;39(1):131-42.
The aim of the present study was to determine the effect of the electrostatic charge of lipoproteins on the phospholipid transfer activity of the plasma phospholipid transfer protein (PLTP). Progressive decreases in the PLTP-mediated phospholipid transfer rates were observed when the surface potential of isolated high density lipoproteins (HDL) was either reduced from -11.7 mV down to -15.7 mV by succinylation of apolipoprotein lysyl residues, or increased from -11.6 mV up to -10.9 mV by replacing apolipoprotein (apo) A-I by apoA-II. When succinylated low density lipoprotein (LDL) series with surface potentials ranging between -4.3 mV and -14.3 mV were used, successive increase and decrease in phospholipid transfer rates were observed along the electronegativity scale. When various plasma HDL subfractions with surface potentials ranging from -10.5 mV to -12.5 mV were separated by anion exchange chromatography, PLTP-mediated phospholipid transfer activity increased progressively with HDL electronegativity until maximal lipid transfer rates were reached for a mean HDL surface potential of -11.6 mV. As the electronegativity of plasma HDL subfractions kept increasing beyond the optimal value, a progressive decrease in PLTP activity was observed. Striking parallelism between cholesteryl ester transfer protein (CETP) and PLTP transfer activity curves obtained with each HDL series were noted, and the optimal HDL surface potential values were remarkably similar, approximating -11.6 mV in all the experiments. With isolated plasma LDL subfractions with surface potentials ranging from -3.5 mV to -5.0 mV, a linear rise in PLTP activity was observed. In conclusion, data of the present study indicate that, like CETP, the activity of PLTP is influenced by electrostatic interactions with lipoproteins.
本研究的目的是确定脂蛋白的静电荷对血浆磷脂转运蛋白（PLTP）磷脂转运活性的影响。当分离的高密度脂蛋白（HDL）的表面电位通过载脂蛋白赖氨酰残基的琥珀酰化作用从-11.7 mV降低至-15.7 mV，或通过用载脂蛋白（apo）A-II替代载脂蛋白A-I从-11.6 mV升高至-10.9 mV时，观察到PLTP介导的磷脂转运速率逐渐降低。当使用表面电位在-4.3 mV至-14.3 mV之间的琥珀酰化低密度脂蛋白（LDL）系列时，沿着电负性尺度观察到磷脂转运速率的连续增加和降低。当通过阴离子交换色谱分离表面电位在-10.5 mV至-12.5 mV之间的各种血浆HDL亚组分时，PLTP介导的磷脂转运活性随着HDL电负性的增加而逐渐增加，直到平均HDL表面电位达到-11.6 mV时达到最大脂质转运速率。当血浆HDL亚组分的电负性继续增加超过最佳值时，观察到PLTP活性逐渐降低。注意到在每个HDL系列中获得的胆固醇酯转运蛋白（CETP）和PLTP转运活性曲线之间存在显著的平行性，并且最佳HDL表面电位值非常相似，在所有实验中均接近-11.6 mV。对于表面电位在-3.5 mV至-5.0 mV之间的分离的血浆LDL亚组分，观察到PLTP活性呈线性上升。总之，本研究数据表明，与CETP一样，PLTP的活性受与脂蛋白静电相互作用的影响。
