Sawamura T, Kume N, Aoyama T, Moriwaki H, Hoshikawa H, Aiba Y, Tanaka T, Miwa S, Katsura Y, Kita T, Masaki T
Department of Pharmacology, Faculty of Medicine, Kyoto University, Japan.
Nature. 1997 Mar 6;386(6620):73-7. doi: 10.1038/386073a0.
Endothelial dysfunction or activation elicited by oxidatively modified low-density lipoprotein (Ox-LDL) has been implicated in the pathogenesis of atherosclerosis, characterized by intimal thickening and lipid deposition in the arteries. Ox-LDL and its lipid constituents impair endothelial production of nitric oxide, and induce the endothelial expression of leukocyte adhesion molecules and smooth-muscle growth factors, which may be involved in atherogenesis. Vascular endothelial cells in culture and in vivo internalize and degrade Ox-LDL through a putative receptor-mediated pathway that does not involve macrophage scavenger receptors. Here we report the molecular cloning, using expression cloning strategy, of an Ox-LDL receptor from vascular endothelial cells. The cloned receptor is a membrane protein that belongs structurally to the C-type lectin family, and is expressed in vivo in vascular endothelium and vascular-rich organs.
氧化修饰的低密度脂蛋白(Ox-LDL)引发的内皮功能障碍或激活与动脉粥样硬化的发病机制有关,其特征是动脉内膜增厚和脂质沉积。Ox-LDL及其脂质成分损害内皮细胞一氧化氮的生成,并诱导白细胞粘附分子和平滑肌生长因子的内皮表达,这些可能参与动脉粥样硬化的发生。培养的和体内的血管内皮细胞通过一种不涉及巨噬细胞清道夫受体的假定受体介导途径内化并降解Ox-LDL。在此,我们报告了使用表达克隆策略从血管内皮细胞中克隆出一种Ox-LDL受体。克隆的受体是一种膜蛋白,在结构上属于C型凝集素家族,在体内血管内皮和血管丰富的器官中表达。