Molecular Pathology in Atherosclerosis: The Mechanism How Cholesteryl Ester Accumulates in Atheromatous Aorta

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  • TAKANO Tatsuya
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • ITABE Hiroyuki
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • MORI Masahiro
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • KIMURA Junji
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • NAKAGAMI Keiji
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • SATO Ryuichiro
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • HASHITA Ryoichi
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • YAGYU Yasuko
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • MINEO Chieko
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • AMANUMA Kimiko
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • IMANAKA Tsuneo
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • HIGASHI Yusuke
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • FUJIMOTO Yasuyuki
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University
  • FUJITA Eiko
    Department of Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University

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Other Title
  • 動脈硬化におけるCholesterolの蓄積粥腫形成・進展機構の分子病理学的解析
  • ドウミャク コウカ ニ オケル Cholesterol ノ チクセキ ジュクシュ ケイセイ シンテン キコウ ノ ブンシ ビョウリガクテキ カイセキ

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Abstract

  To study how cholesterol accumulates in atheroma, novel monoclonal antibodies were developed, using crude homogenate of atheroma as immunogens. 212D monoclonal antibody recognizing extra cellular matrix with lipid-laden deposits was selected by histochemical staining. The antigen was deduced vitronectin from cDNA library. DLH3 monoclonal antibody recognizing oxidized LDL, epitope of which was 5- or 9-phosphatidylcholine. Significant correlations between oxidized LDL and coronary heart disease (CHD) patients were observed from clinical study. 256C monoclonal antibody recognizing atheromatous lesions in human aorta was selected. Epitope must be PC-cholesterol complex which may involve in foam cell rupture. Atherogenesis will be discussed from the aspects of these antibodies. Our working hypothesis is required to elucidate the mechanism. Denatured lipoproteins (either oxidized lipoprotein or ruptured foam cells) may induce atheroma. Oxidation of lipoprotein may be taken place both in foam cells and/or extra cellular matrix, and macrophage eliminate these denatured lipoproteins and become foam cells. The foam cells are ruptured by either apoptosis or necrosis afterward, and hydrophobic fragments of foam cells dispersed in extra cellular space, which destroys the function of biological membrane. Since biological function could be maintained by segregation of hydrophilic circumstances, macrophages uptake these fragmented material and oxidized lipoprotein to maintain the function. This vicious spiral may enhance chronically the atheroma.<br>

Journal

  • YAKUGAKU ZASSHI

    YAKUGAKU ZASSHI 128 (10), 1383-1401, 2008-10-01

    The Pharmaceutical Society of Japan

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