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An immunohistochemical study of human platelets using a rabbit antibody against H18-K24 of apolipoprotein CIII (HATKTAK)

Authors

  • Takao Yamanaka,

    1. Inflammation Pathology, Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa, Japan
    2. Internal Medicine, Minami-Okayama Medical Center, Incorporated Administrative Agency National Hospital Organization, Okayama, Japan
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  • Haruhiko Sakamoto,

    Corresponding author
    • Inflammation Pathology, Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa, Japan
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  • Toshitaka Nakagawa,

    1. Division of Research Instrument and Equipment, Life Science Research Center, Institute of Research Promotion, Kagawa University, Kagawa, Japan
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  • Sumiko Tanaka,

    1. Inflammation Pathology, Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa, Japan
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  • Kouichi Matsumoto,

    1. Inflammation Pathology, Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa, Japan
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  • Masaki Ueno

    1. Inflammation Pathology, Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa, Japan
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Correspondence: Haruhiko Sakamoto, MD, PhD, Inflammation Pathology, Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa 761-0793, Japan. Email: profsaka@med.kagawa-u.ac.jp

Abstract

H18-K24 of human apolipopotein CIII (Apo CIII) (HATKTAK) is an activator of the macromolecular activators of phagocytosis from platelets (MAPPs). Using a rabbit antibody against HATKTAK, we performed an immunohistochemical study of human platelets. Indirect ELISA showed that this antibody reacts with Apo CIII-derived peptides with a C-terminal of HATKTAK, but not with Apo CIII. Immunoelectron microscopy revealed that reaction of anti-HATKTAK antibody occurred in the pseudopods of activated platelets. In blood coagula produced from the peripheral blood and formalin-fixed after various incubation periods, reaction of this antibody with platelets appeared rapidly with a peak at 3 to 6 h of incubation, and then diminished gradually. Leukocytes in the blood coagula were stained strongly positive. In tissue sections, fresh thrombi and hemorrhages with slight fibrin formation revealed a positive response of platelets to anti-HATKTAK antibody, whereas older ones with leukocytic infiltration, fibrin formation and organization did not. In addition to platelets, endothelial cells and leukocytes were stained positive by anti-HATKTAK antibody. All of the positive reactions by anti-HATKTAK antibody disappeared or diminished by co-incubation with HATKTAK. In conclusion, the anti-HATKTAK antibody reveals platelets during the early phase of activation.

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