Improvement of Anemia Associated with Chronic Renal Failure by Recombinant Human Erythropoietin Treatment in 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
    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
  • ANAN Sayuri
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • MIYAMOTO Keiko
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • MIYAMOTO Youhei
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • 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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Abstract

The ICR-derived glomerulonephritis (ICGN) mouse, a novel inbred mouse strain with a hereditary nephrotic syndrome, develops severe anemia associated with chronic renal failure. To reveal the pathogenic mechanism of anemia in ICGN mice, we subcutaneously administered recombinant human erythropoietin (rhEPO; 5 IU/mouse/day) or saline for 5 days to ICGN mice. In terminal-stage ICGN mice with severe anemia, rhEPO significantly increased hematocrit (Ht), red blood cells (RBC) and hemoglobin levels. Endogenous EPO levels in peripheral blood were reduced by rhEPO injection. No histopathological changes in bone marrow and kidneys were induced by rhEPO injection. Insufficiency of EPO may cause anemia in ICGN mice.<br>

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