A mouse model of adult-onset anaemia due to erythropoietin deficiency

Shun Yamazaki, Tomokazu Souma, Ikuo Hirano, Xiaoqing Pan, Naoko Minegishi, Norio Suzuki () and Masayuki Yamamoto ()
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Shun Yamazaki: Tohoku University Graduate School of Medicine
Tomokazu Souma: Tohoku University Graduate School of Medicine
Ikuo Hirano: Tohoku University Graduate School of Medicine
Xiaoqing Pan: Tohoku University Graduate School of Medicine
Naoko Minegishi: Tohoku University Graduate School of Medicine
Norio Suzuki: United Centers for Advanced Research and Translational Medicine, Tohoku University Graduate School of Medicine
Masayuki Yamamoto: Tohoku University Graduate School of Medicine

Nature Communications, 2013, vol. 4, issue 1, 1-12

Abstract: Abstract Erythropoietin regulates erythropoiesis in a hypoxia-inducible manner. Here we generate inherited super-anaemic mice (ISAM) as a mouse model of adult-onset anaemia caused by erythropoietin deficiency. ISAM express erythropoietin in the liver but lack erythropoietin production in the kidney. Around weaning age, when the major erythropoietin-producing organ switches from the liver to the kidney, ISAM develop anaemia due to erythropoietin deficiency, which is curable by administration of recombinant erythropoietin. In ISAM severe chronic anaemia enhances transgenic green fluorescent protein and Cre expression driven by the complete erythropoietin-gene regulatory regions, which facilitates efficient labelling of renal erythropoietin-producing cells. We show that the majority of cortical and outer medullary fibroblasts have the innate potential to produce erythropoietin, and also reveal a new set of erythropoietin target genes. ISAM are a useful tool for the evaluation of erythropoiesis-stimulating agents and to trace the dynamics of erythropoietin-producing cells.

Date: 2013
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DOI: 10.1038/ncomms2950

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