Zhang C, Akira M, Hideki H, Hisashi S, Seikoh H
Department of Medical Laboratory Science, Nanjing General Hospital of PLA, Nanjing 210002, China.
Chin Med J (Engl). 1999 Jun;112(6):543-5.
To investigate the atherogenic role of very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) fraction isolated from plasma of apolipoprotein E (apoE)-knockout mice.
Containing both VLDL and IDL (apoEko-VLDL/IDL), lipoprotein fraction was isolated from plasma of apoE-knockout mice by ultracentrifugation, and its interaction with J774 macrophages was examined together with its physicochemical properties including lipid content, electrophoresis mobility and apolipoprotein components.
ApoEko-VLDL/IDL could be actively taken up by J774 macrophages, resulting in marked cholesterol ester accumulation in the cells (55 +/- 9 nmol/mg cell protein), which was a 7-fold increase over the corresponding lever induced by low density lipoprotein and significantly higher than non-loaded group (P < 0.01).
ApoEko-VLDL/IDL induced significant cholesterol ester accumulation through an apoE independent pathway. This pathway may explain, partly the mechanism of cholesterol deposition in arterial wall in apoE-knockout mice.
研究从载脂蛋白E（apoE）基因敲除小鼠血浆中分离出的极低密度脂蛋白（VLDL）和中间密度脂蛋白（IDL）组分的致动脉粥样硬化作用。
通过超速离心从apoE基因敲除小鼠血浆中分离出同时含有VLDL和IDL的脂蛋白组分（apoEko-VLDL/IDL），并检测其与J774巨噬细胞的相互作用以及包括脂质含量、电泳迁移率和载脂蛋白成分在内的物理化学性质。
ApoEko-VLDL/IDL可被J774巨噬细胞主动摄取，导致细胞内显著的胆固醇酯积累（55±9 nmol/mg细胞蛋白），这比低密度脂蛋白诱导的相应水平增加了7倍，且显著高于未加载组（P<0.01）。
ApoEko-VLDL/IDL通过不依赖apoE的途径诱导显著的胆固醇酯积累。该途径可能部分解释了apoE基因敲除小鼠动脉壁胆固醇沉积的机制。
