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PNAS 98 (15): 8780-8785

Copyright © 2001 by the National Academy of Sciences.

From the Cover


BIOLOGICAL SCIENCES / MEDICAL SCIENCES

Lack of hepcidin gene expression and severe tissue iron overload in upstream stimulatory factor 2 (USF2) knockout mice

Gaël Nicolas*, Myriam Bennoun*, Isabelle Devaux{dagger}, Carole Beaumont{dagger}, Bernard Grandchamp{dagger}, Axel Kahn*, and Sophie Vaulont*,{ddagger}

*Institut National de la Santé et de la Recherche Médicale 129, Departement Genetique Developpement et Pathologie Moléculaire, Institut Cochin de Genetique Moléculaire, Faculté de Médecine Cochin-Port Royal, 75014 Paris, France; and {dagger}Institut National de la Santé et de la Recherche Médicale 409, Faculté de Médecine Xavier Bichat, 75018 Paris, France

Received for publication April 11, 2001.

Abstract: We previously reported the disruption of the murine gene encoding the transcription factor USF2 and its consequences on glucose-dependent gene regulation in the liver. We report here a peculiar phenotype of Usf2–/– mice that progressively develop multivisceral iron overload; plasma iron overcomes transferrin binding capacity, and nontransferrin-bound iron accumulates in various tissues including pancreas and heart. In contrast, the splenic iron content is strikingly lower in knockout animals than in controls. To identify genes that may account for the abnormalities of iron homeostasis in Usf2–/– mice, we used suppressive subtractive hybridization between livers from Usf2–/– and wild-type mice. We isolated a cDNA encoding a peptide, hepcidin (also referred to as LEAP-1, for liver-expressed antimicrobial peptide), that was very recently purified from human blood ultrafiltrate and from urine as a disulfide-bonded peptide exhibiting antimicrobial activity. Accumulation of iron in the liver has been recently reported to up-regulate hepcidin expression, whereas our data clearly show that a complete defect in hepcidin expression is responsible for progressive tissue iron overload. The striking similarity of the alterations in iron metabolism between HFE knockout mice, a murine model of hereditary hemochromatosis, and the Usf2–/– hepcidin-deficient mice suggests that hepcidin may function in the same regulatory pathway as HFE. We propose that hepcidin acts as a signaling molecule that is required in conjunction with HFE to regulate both intestinal iron absorption and iron storage in macrophages.


{ddagger} To whom reprint requests should be addressed. E-mail: vaulont{at}cochin.inserm.fr.

Edited by William S. Sly, Saint Louis University School of Medicine, St. Louis, MO, and approved May 10, 2001

This paper was submitted directly (Track II) to the PNAS office.

See commentary on page 8160.

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J. Am. Soc. Nephrol. 18, 394-400
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Increased plasma transferrin, altered body iron distribution, and microcytic hypochromic anemia in ferrochelatase-deficient mice.
S. Lyoumi, M. Abitbol, V. Andrieu, D. Henin, E. Robert, C. Schmitt, L. Gouya, H. de Verneuil, J.-C. Deybach, X. Montagutelli, et al. (2007)
Blood 109, 811-818
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Cis and trans regulation of hepcidin expression by upstream stimulatory factor.
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Blood 108, 4237-4245
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Hepcidin and the anemia of chronic disease..
F. I. Haurani (2006)
Ann. Clin. Lab. Sci. 36, 3-6
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