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Blood, 15 February 2006, Vol. 107, No. 4, pp. 1659-1664. Prepublished online as a Blood First Edition Paper on October 20, 2005; DOI 10.1182/blood-2005-07-2614. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-07-2614v1 107/4/1659    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Wilkins, S. J. Articles by Anderson, G. J. Search for Related Content PubMed PubMed Citation Articles by Wilkins, S. J. Articles by Anderson, G. J. Related Collections Red Cells Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Iron metabolism in the hemoglobin-deficit mouse: correlation of diferric transferrin with hepcidin expression Sarah J. Wilkins, David M. Frazer, Kirstin N. Millard, Gordon D. McLaren, and Gregory J. Anderson From the Iron Metabolism Laboratory, The Queensland Institute of Medical Research, Brisbane, Australia; and the VA Long Beach Healthcare System, Long Beach, and Division of Hematology/Oncology, University of California, Irvine. The iron requirements of the erythroid compartment modulate the expression of hepcidin in the liver, which in turn alters intestinal iron absorption and iron release from the reticuloendothelial system. We have taken advantage of an inherited anemia of the mouse (hemoglobin deficit, or hbd) to gain insights into the factors regulating hepcidin expression. hbd mice showed a significant anemia but, surprisingly, their iron absorption was not increased as it was in wild-type animals made anemic to a similar degree by dietary iron depletion. In wild-type mice hepatic hepcidin levels were decreased but in hbd animals a significant and unexpected increase was observed. The level of absorption was appropriate for the expression of hepcidin in each case, but in hbd mice did not reflect the degree of anemia. However, this apparent inappropriate regulation of hepcidin correlated with increased transferrin saturation and levels of diferric transferrin in the plasma, which in turn resulted from the reduced capacity of hbd animals to effectively use transferrin-bound iron. These data strengthen the proposal that diferric transferrin is a key indicator of body iron requirements. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Trombini, T. Coliva, E. Nemeth, R. Mariani, T. Ganz, A. Biondi, and A. Piperno Effects of plasma transfusion on hepcidin production in human congenital hypotransferrinemia Haematologica, October 1, 2007; 92(10): 1407 - 1410. [Abstract] [Full Text] [PDF] L. Lin, E. V. Valore, E. Nemeth, J. B. Goodnough, V. Gabayan, and T. Ganz Iron transferrin regulates hepcidin synthesis in primary hepatocyte culture through hemojuvelin and BMP2/4 Blood, September 15, 2007; 110(6): 2182 - 2189. [Abstract] [Full Text] [PDF] A. T. Murphy, D. R. Witcher, P. Luan, and V. J. Wroblewski Quantitation of hepcidin from human and mouse serum using liquid chromatography tandem mass spectrometry Blood, August 1, 2007; 110(3): 1048 - 1054. [Abstract] [Full Text] [PDF] T. Goswami and N. C. Andrews Hereditary Hemochromatosis Protein, HFE, Interaction with Transferrin Receptor 2 Suggests a Molecular Mechanism for Mammalian Iron Sensing J. Biol. Chem., September 29, 2006; 281(39): 28494 - 28498. [Abstract] [Full Text] [PDF]

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