Dysfunction of Erythropoietin-Producing Interstitial Cells in the Kidneys of ICR-derived Glomerulonephritis (ICGN) Mice

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  • YAMAGUCHI-YAMADA Misuzu
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • MANABE Noboru
    Research Unit for Animal Life Sciences, Animal Resource Science Center, The University of Tokyo
  • KISO Minako
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • GOTO Yasufumi
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University Research Unit for Animal Life Sciences, Animal Resource Science Center, The University of Tokyo
  • MORI Toshiharu
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • SAKATA Chinatsu
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • ANAN Sayuri
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University Research Unit for Animal Life Sciences, Animal Resource Science Center, The University of Tokyo
  • NAGAO Masaya
    Laboratory of Biosignals and Response, Department of Applied Molecular Biology, Kyoto University
  • YAMAMOTO Yoshie
    Department of Veterinary Sciences, National Institute of Infectious Diseases
  • OGURA Atsuo
    Bioresource Center, RIKEN

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Anemia is a major secondary symptom in chronic renal disorder (CRD), but the precise cause of insufficient production of erythropoietin (EPO) remains unclear owing to the controversial localization of EPO-producing cells in the kidneys. The ICR-derived glomerulonephritis (ICGN) mouse, a new hereditary nephrotic mouse, is an appropriate model of anemia associated with CRD. By using an amplified in situ hybridization technique, we detected and counted the renal EPO-producing cells under both normoxic and hypoxic conditions. The expression levels of renal EPO mRNA were quantified and oxygen gradients were also assessed immunohistochemically. Amplified in situ hybridization clarified that EPO-producing cells were peritubular interstitial cells in the middle region of renal cortex in both ICR and ICGN mice. Hypoxia (7% O2) induced low oxygen tension in proximal tubular epithelial cells of renal cortex, and increased the expression of EPO mRNA and the number of EPO-producing cells in both ICR and ICGN mice. However, hypoxia did not increase the serum EPO levels in ICGN mice. The ICGN mouse is a good model for anemia associated with CRD, and the suppression of EPO protein production in the renal EPO-producing cells is considered to be a potential cause of anemia associated with CRD.<br>

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