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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.
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RED CELLS
Brief report
Deregulation of proteins involved in iron metabolism in hepcidin-deficient mice
Lydie Viatte,
Jeanne-Claire Lesbordes-Brion,
Dan-Qing Lou,
Myriam Bennoun,
Gaël Nicolas,
Axel Kahn,
François Canonne-Hergaux, and
Sophie Vaulont
From the Institut National de la Santé et de la Recherche Médicale 567, Centre National de la Recherche Scientifique, et Université René Descartes, Institut Cochin, Faculté deMédecine Cochin-Port Royal, Paris, France; and the Institut National de la Santé et de la Recherche Médicale 409, Faculté de médecine Xavier Bichat, Paris, France.
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 cytochrome b (Dcytb), divalent metal transporter 1 (DMT1), and ferroportin compared with 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. We hypothesized that the deregulation of these proteins might be central in the pathogenesis of iron overload, providing key therapeutic targets for iron disorders. (Blood. 2005;105:4861-4864)
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