Amyloidosis-inducing activity of blood cells in mouse AApoAII amyloidosis

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  • Ding Xin
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Liu Yingye
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Yang Mu
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Li Lin
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Miyahara Hiroki
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Dai Jian
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Xu Zhe
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Matsumoto Kiyoshi
    Division of Animal Research, Research Center for Supports to Advanced Science, Shinshu University, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Mori Masayuki
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan Department of Advanced Medicine for Health Promotion, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Higuchi Keiichi
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan Department of Biological Sciences for Intractable Neurological Diseases, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan
  • Sawashita Jinko
    Department of Aging Biology, Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan Department of Biological Sciences for Intractable Neurological Diseases, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, 3-1-1 Asahi, Matsumoto-shi, Nagano 390-8621, Japan

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Abstract

<p> Mouse senile amyloidosis is a disorder in which apolipoprotein A-II (APOA2) deposits as amyloid fibrils (AApoAII) in many organs. We previously reported that AApoAII amyloidosis can be transmitted by feces, milk, saliva and muscle originating from mice with amyloid deposition. In this study, the ability of blood components to transmit amyloidosis was evaluated in our model system. Blood samples were collected from SAMR1.SAMP1-Apoa2c amyloid-laden or amyloidosis-negative mice. The samples were fractionated into plasma, white blood cell (WBC) and red blood cell (RBC) fractions. Portions of each were further separated into soluble and insoluble fractions. These fractions were then injected into recipient mice to determine amyloidosis-induction activities (AIA). The WBC and RBC fractions from amyloid-laden mice but not from amyloidosis-negative mice induced AApoAII amyloid deposition in the recipients. The AIA of WBC fraction could be attributed to AApoAII amyloid fibrils because amyloid fibril-like materials and APOA2 antiserum-reactive proteins were observed in the insoluble fraction of the blood cells. Unexpectedly, the plasma of AApoAII amyloidosis-negative as well as amyloid-laden mice showed AIA, suggesting the presence of substances in mouse plasma other than AApoAII fibrils that could induce amyloid deposition. These results indicated that AApoAII amyloidosis could be transmitted across tissues and between individuals through blood cells.</p>

Journal

  • Experimental Animals

    Experimental Animals 67 (2), 105-115, 2018

    Japanese Association for Laboratory Animal Science

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