Species differences of macrophage very low-density-lipoprotein (VLDL) receptor protein expression
Species differences of macrophage very low-density-lipoprotein (VLDL) receptor protein expression
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DOI：
10.1016/j.bbrc.2011.03.069
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发表时间：
2011-04-22
影响因子：
3.1
通讯作者：
Shiomi, Masashi
中科院分区：
文献类型：
--
作者：
Takahashi, Sadao;Ito, Takashi;Shiomi, Masashi
富含甘油三酯的脂蛋白（TGRL）和低密度脂蛋白（LDL）胆固醇是冠状动脉疾病的独立危险因素。我们先前提出极低密度脂蛋白（VLDL）受体是人类巨噬细胞中TGRLs形成泡沫细胞所需的受体之一。然而，VLDL受体蛋白尚未在几种动物模型的动脉粥样硬化病变中检测到。在此，我们发现在小鼠巨噬细胞系（Raw 264.7和J774.2）或体外小鼠腹腔巨噬细胞中未检测到VLDL受体蛋白。此外，在体内喂食普通饲料的载脂蛋白E缺陷小鼠或喂食胆固醇的低密度脂蛋白受体缺陷小鼠的动脉粥样硬化病变中的巨噬细胞中未检测到VLDL受体蛋白。与此相反，巨噬细胞VLDL受体蛋白在体外人巨噬细胞和心肌梗死倾向的Watanabe遗传性高脂血症（WHHLMI）兔体内动脉粥样硬化病变中明确检测到。VLDL受体蛋白在体内外的定位存在种属差异。由于VLDL受体在兔和人的动脉粥样硬化斑块中的巨噬细胞上表达，而在小鼠模型中不表达，因此小鼠模型中动脉粥样硬化形成和/或动脉粥样硬化病变生长的机制可能与人和兔的机制部分不同。(C)2011 Elsevier Inc. All rights reserved.
Triglyceride-rich lipoproteins (TGRLs) and low-density-lipoprotein (LDL) cholesterol are independent risk factors for coronary artery disease. We have previously proposed that the very low-density-lipoprotein (VLDL) receptor is one of the receptors required for foam cell formation by TGRLs in human macrophages. However, the VLDL receptor proteins have not been detected in atherosclerotic lesions of several animal models. Here we showed no VLDL receptor protein was detected in mouse macrophage cell lines (Raw264.7 and J774.2) or in mouse peritoneal macrophages in vitro. Furthermore, no VLDL receptor protein was detected in macrophages in atherosclerotic lesions of chow-fed apolipoprotein E-deficient or cholesterol-fed LDL receptor-deficient mice in vivo. In contrast, macrophage VLDL receptor protein was clearly detected in human macrophages in vitro and in atherosclerotic lesions in myocardial infarction-prone Watanabe-heritable hyperlipidemic (WHHLMI) rabbits in vivo. There are species differences in the localization of VLDL receptor protein in vitro and in vivo. Since VLDL receptor is expressed on macrophages in atheromatous plaques of both rabbit and human but not in mouse models, the mechanisms of atherogenesis and/or growth of atherosclerotic lesions in mouse models may be partly different from those of humans and rabbits. (C) 2011 Elsevier Inc. All rights reserved.