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Species differences of macrophage very low-density-lipoprotein (VLDL) receptor protein expression
Authors:Takahashi Sadao  Ito Takashi  Zenimaru Yasuo  Suzuki Jinya  Miyamori Isamu  Takahashi Masao  Takahashi Masafumi  Ishida Takafumi  Ishida Tatsuro  Hirata Ken-Ichi  Yamamoto Tokuo T  Iwasaki Tadao  Hattori Hiroaki  Shiomi Masashi
Institution:aThird Department of Internal Medicine, University of Fukui, Faculty of Medical Science, Japan;bResearch and Education Program for Life Science, University of Fukui, Faculty of Medical Science, Japan;cInstitute for Experimental Animals, Kobe University Graduate School of Medicine, Japan;dDepartment of Cardiovascular Surgery, Hiratsuka Kyosai Hospital, Japan;eDivision of Bioimaging Sciences, Center for Molecular Medicine, Jichi Medical University, Japan;fDepartment of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical Sciences, Japan;gDivision of Cardiovascular Medicine, Kobe University Graduate School of Medicine, Japan;hCenter for Advanced Genome Research, Institute of Development, Aging, and Cancer, Tohoku University, Japan;iDepartment of Advanced Medical Technology and Development, BML, Inc., Japan;jSection of Animal Models for Cardiovascular Diseases, Kobe University Graduate School of Medicine, Japan
Abstract: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.
Keywords:Abbreviations: TGRLs  triglyceride-rich lipoproteins  VLDL  very low-density lipoprotein  LDL  low-density-lipoprotein  WHHLMI  myocardial infarction-prone Watanabe-heritable hyperlipidemic  apo  apolipoprotein  CADs  coronary artery diseases
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