ApoE基因摧毁鼠VLDL/IDL组分诱导J774巨噬细胞胆固醇酯蓄积

Very low and intermediate density lipoprotein fraction from apolipoprotein E-knockout mice induce cholesterol ester accumulation in J774 macrophages

目的：探讨ａｐｏＥ 基因摧毁鼠血浆极低密度脂蛋白和中间密度脂蛋白组分（ａｐｏＥｋｏ － ＶＬＤＬ／ＩＤＬ） 致动脉硬化作用。方法：检测ａｐｏＥｋｏ － ＶＬＤＬ／ＩＤＬ 的理化性质，包括脂含量，电泳迁移率和载脂蛋白组成，并观察了该组分与Ｊ７７４巨噬细胞的相互作用。结果：ａｐｏＥｋｏ － ＶＬＤＬ／ＩＤＬ 可被Ｊ７７４ 巨噬细胞摄取，导致细胞胆固醇酯（ＣＥ） 大量蓄积（ Ｐ＜０－０１） 。结论：ａｐｏＥ 缺失鼠血浆非修饰ａｐｏＥｋｏ － ＶＬＤＬ／ＩＤＬ 组分以不依赖ａｐｏＥ 方式转Ｊ７７４ 巨噬细胞为泡沫细胞。

AIM: To investigate the atherogenic role of VLDL and IDL fraction isolated from plasma of lipoproteins E-knockout mice. METHODS: The lipoprotein fraction containing both VLDL and IDL fraction (apoEko-VLDL/IDL) 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. RESULTS: The 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 an 7-fold increase over the corresponding lever induced by low density lipoprotein and significantly higher than non-loaded group( P <0.01). CONCLUSION: Unmodified apoEko-VLDL/IDL fraction transferred J774 macrophages to foam cells through an apoE independent pathway.