Thorne Rick F, Mhaidat Nizar M, Ralston Kylie J, Burns Gordon F
Cancer Research Unit, School of Biomedical Science, Faculty of Health, The University of Newcastle, NSW 2308, Australia.
FEBS Lett. 2007 Mar 20;581(6):1227-32. doi: 10.1016/j.febslet.2007.02.043. Epub 2007 Feb 28.
Atherosclerotic plaques result from the excessive deposition of cholesterol esters derived from lipoproteins and lipoprotein fragments. Tissue macrophage within the intimal space of major arterial vessels have been shown to play an important role in this process. We demonstrate in a transfection system using two human cell lines that the macrophage scavenger receptor CD36 selectively elicited lipid uptake from Cu(2+)-oxidized high density lipoprotein (HDL) but not from native HDL or low density lipoprotein (LDL). The uptake of oxHDL displayed morphological and biochemical similarities with the CD36-dependent uptake of oxidized LDL. CD36-mediated uptake of oxidized HDL by macrophage may therefore contribute to atheroma formation.
动脉粥样硬化斑块是由脂蛋白和脂蛋白片段衍生的胆固醇酯过度沉积所致。主要动脉血管内膜空间内的组织巨噬细胞已被证明在这一过程中起重要作用。我们在使用两种人类细胞系的转染系统中证明，巨噬细胞清道夫受体CD36选择性地引发从铜（2+）氧化的高密度脂蛋白（HDL）摄取脂质，但不从天然HDL或低密度脂蛋白（LDL）摄取脂质。氧化HDL的摄取在形态和生化方面与CD36依赖的氧化LDL摄取相似。因此，巨噬细胞通过CD36介导摄取氧化HDL可能有助于动脉粥样硬化的形成。
