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

Misuzu YAMAGUCHI-YAMADA; Noboru MANABE; Minako KISO; Yasufumi GOTO; Toshiharu MORI; Chinatsu SAKATA; Sayuri ANAN; Masaya NAGAO; Yoshie YAMAMOTO; Atsuo OGURA

doi:10.1292/jvms.67.891

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

Misuzu YAMAGUCHI-YAMADA, Noboru MANABE, Minako KISO, Yasufumi GOTO, Toshiharu MORI, Chinatsu SAKATA, Sayuri ANAN, Masaya NAGAO, Yoshie YAMAMOTO, Atsuo OGURA

Author information

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

Keywords: amplified in situ hybridization, anemia with chronic renal disorder (CRD), erythropoietin (EPO)-producing cell, hereditary nephrotic ICR-derived glomerulonephritis (ICGN) mouse, kidney

JOURNAL FREE ACCESS

2005 Volume 67 Issue 9 Pages 891-899

DOI https://doi.org/10.1292/jvms.67.891

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Abstract

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.

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