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Blood, 1 April 2004, Vol. 103, No. 7, pp. 2816-2821. Prepublished online as a Blood First Edition Paper on November 6, 2003; DOI 10.1182/blood-2003-07-2524. This Article Full Text (PDF) All Versions of this Article: 2003-07-2524v1 103/7/2816    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 Lou, D.-Q. Articles by Vaulont, S. Search for Related Content PubMed PubMed Citation Articles by Lou, D.-Q. Articles by Vaulont, S. Social Bookmarking                   What's this? Submitted July 25, 2003 Accepted October 23, 2003 Functional differences between hepcidin-1 and -2 in transgenic mice Dan-Qing Lou, Gael Nicolas, Jeanne-Claire Lesbordes, Lydie Viatte, Gisele Grimber, Marie-France Szajnert, Axel Kahn, and Sophie Vaulont* Departement Genetique, Developpement et Pathologie Moleculaire, Institut Cochin, Paris, France INSERM, Unite 409, Faculte Xavier Bichat, Paris, France * Corresponding author; email: vaulont{at}cochin.inserm.fr. Hepcidin is a 25-amino-acid peptide involved in iron homeostasis in mice and humans. It is produced in the liver from a larger precursor and it is detectable in blood and urine. In contrast to the human genome which contains only one copy of the gene, the mouse genome contains two highly similar hepcidin genes, hepc1 and hepc2, which are, however, considerably divergent at the level of the corresponding mature 25-amino-acid peptide. This striking observation led us to ask whether hepc1 and hepc2 performed the same biological activity with regard to iron metabolism in the mouse. We recently described the severe iron-deficient anemia phenotype in transgenic mice overexpressing hepc1 in the liver. Here we report that, in contrast to the hepc1transgenic mice, none of the seven founder hepc2-transgenic animals suffered from anemia. They all developed normally with hematological parameters similar to the non-transgenic littermates. Hepc2 transgenic mRNA level was found to be very high for all lines compared with the level of hepc1 transgene mRNA necessary to produce severe anemia. These data provide evidence that hepc2 does not act on iron metabolism like hepc1, and give clues for the identification of amino acids important for the iron-regulatory action of the mature 25-amino-acid peptide. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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