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Blood, 15 June 2005, Vol. 105, No. 12, pp. 4861-4864. Prepublished online as a Blood First Edition Paper on February 15, 2005; DOI 10.1182/blood-2004-12-4608. This Article Full Text (PDF) All Versions of this Article: 2004-12-4608v1 105/12/4861    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Viatte, L. Articles by Vaulont, S. Search for Related Content PubMed PubMed Citation Articles by Viatte, L. Articles by Vaulont, S. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 2, 2004 Accepted February 3, 2005 Deregulation of proteins involved in iron metabolism in hepcidin-deficient mice Lydie Viatte, Jeanne-Claire Lesbordes-Brion, Dan-Qing Lou, Myriam Bennoun, Gael Nicolas, Axel Kahn, Francois Canonne-Hergaux, and Sophie Vaulont* Institut National de la Sante et de la Recherche Medicale 567, Centre National de la Recherche Scientifique, et Universite Rene Descartes, Institut Cochin, Faculte de Medecine Cochin Port-Royal, Paris, France Institut National de la Sante et de la Recherche Medicale 409, Faculte de medecine Xavier Bichat 75018, Paris, France * Corresponding author; email: vaulont{at}cochin.inserm.fr. Evidence is accumulating that hepcidin, a liver regulatory peptide, could be the common pathogenetic denominator of all forms of iron overload syndromes including HFE-related hemochromatosis, the most prevalent genetic disorder characterized by inappropriate iron absorption. To understand the mechanisms whereby hepcidin controls iron homeostasis in vivo, we have analyzed the level of iron-related proteins by Western blot and immunohistochemistry in hepcidin-deficient mice, a mouse model of severe hemochromatosis. These mice showed important increased levels of duodenal Dcytb, DMT1 and ferroportin as compared to control mice. Interestingly, the level of ferroportin was coordinately up-regulated in the duodenum, the spleen and the liver (predominantly in the Kupffer cells). Finally, we also evidenced a decrease of ceruloplasmin in the liver of hepcidin-deficient mice. 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