SEARCH:   Advanced

Prepublished online as a Blood First Edition Paper on April 30, 2002; DOI 10.1182/blood-2001-11-0037. This Article Full Text Full Text (PDF) All Versions of this Article: 2001-11-0037v1 100/4/1465    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 Ajioka, R. S. Articles by Kushner, J. P. Search for Related Content PubMed PubMed Citation Articles by Ajioka, R. S. Articles by Kushner, J. P. Related Collections Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 August 2002, Vol. 100, No. 4, pp. 1465-1469 RED CELLS Regulation of iron absorption in Hfe mutant mice Richard S. Ajioka, Joanne E. Levy, Nancy C. Andrews, and James P. Kushner From the Division of Hematology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City; the Division of Hematology/ Oncology, Children's Hospital, Department of Pediatrics, Harvard University, Cambridge, MA; Howard Hughes Medical Institute, Chevy Chase, MD; and the Division of Hematology, Brigham and Women's Hospital, Boston, MA. Hereditary hemochromatosis is most commonly caused by homozygosity for a point mutation (C282Y) in the human hemochromatosis gene (HFE). The mechanism by which HFE regulates iron absorption is not known, but the C282Y mutation results in loss of cell surface expression of the human hemachromatosis protein (HFE) and hyperabsorption of iron by the duodenal enterocyte. Mice homozygous for a deletion in the mouse hemochromatosis gene (Hfe) or a mutation equivalent to that seen in human hereditary hemochromatosis (C282Y) were compared with wild-type animals for their ability to regulate iron absorption. Both mutant strains hyperabsorbed 59Fe administered by gavage. Feeding a diet supplemented with carbonyl iron resulted in a more than 5-fold reduction of 59Fe absorption in both wild-type and mutant mouse strains. Similarly, the iron loading associated with age in Hfe mutant mice resulted in nearly a 4-fold reduction in iron absorption. When mice were stimulated to absorb iron either by depleting iron stores or by inducing erythropoiesis, wild type and Hfe mutant strains increased absorption to similar levels, approximately 5-fold over control values. Our data indicate that Hfe mutant mice retain the ability to regulate iron absorption. Mouse hemachromatosis protein (Hfe) plays a minor role in down-regulation but does not influence the up-regulation of iron absorption. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. Kautz, D. Meynard, C. Besson-Fournier, V. Darnaud, T. Al Saati, H. Coppin, and M.-P. Roth BMP/Smad signaling is not enhanced in Hfe-deficient mice despite increased Bmp6 expression Blood, September 17, 2009; 114(12): 2515 - 2520. [Abstract] [Full Text] [PDF] M. Constante, D. Wang, V.-A. Raymond, M. Bilodeau, and M. M. Santos Repression of Repulsive Guidance Molecule C during Inflammation Is Independent of Hfe and Involves Tumor Necrosis Factor-{alpha} Am. J. Pathol., February 1, 2007; 170(2): 497 - 504. [Abstract] [Full Text] [PDF] S. F. Drake, E. H. Morgan, C. E. Herbison, R. Delima, R. M. Graham, A. C. G. Chua, P. J. Leedman, R. E. Fleming, B. R. Bacon, J. K. Olynyk, et al. Iron absorption and hepatic iron uptake are increased in a transferrin receptor 2 (Y245X) mutant mouse model of hemochromatosis type 3 Am J Physiol Gastrointest Liver Physiol, January 1, 2007; 292(1): G323 - G328. [Abstract] [Full Text] [PDF] J.-C. Lesbordes-Brion, L. Viatte, M. Bennoun, D.-Q. Lou, G. Ramey, C. Houbron, G. Hamard, A. Kahn, and S. Vaulont Targeted disruption of the hepcidin 1 gene results in severe hemochromatosis Blood, August 15, 2006; 108(4): 1402 - 1405. [Abstract] [Full Text] [PDF] M. Constante, W. Jiang, D. Wang, V.-A. Raymond, M. Bilodeau, and M. M. Santos Distinct requirements for Hfe in basal and induced hepcidin levels in iron overload and inflammation Am J Physiol Gastrointest Liver Physiol, August 1, 2006; 291(2): G229 - G237. [Abstract] [Full Text] [PDF] C. Camaschella Understanding iron homeostasis through genetic analysis of hemochromatosis and related disorders Blood, December 1, 2005; 106(12): 3710 - 3717. [Abstract] [Full Text] [PDF] D. M. Frazer and G. J. Anderson Iron Imports. I. Intestinal iron absorption and its regulation Am J Physiol Gastrointest Liver Physiol, October 1, 2005; 289(4): G631 - G635. [Abstract] [Full Text] [PDF] H. Makui, R. J. Soares, W. Jiang, M. Constante, and M. M. Santos Contribution of Hfe expression in macrophages to the regulation of hepatic hepcidin levels and iron loading Blood, September 15, 2005; 106(6): 2189 - 2195. [Abstract] [Full Text] [PDF] A. C. G. Chua, J. K. Olynyk, P. J. Leedman, and D. Trinder Nontransferrin-bound iron uptake by hepatocytes is increased in the Hfe knockout mouse model of hereditary hemochromatosis Blood, September 1, 2004; 104(5): 1519 - 1525. [Abstract] [Full Text] [PDF] T Kelleher, E Ryan, S Barrett, M Sweeney, V Byrnes, C O'Keane, and J Crowe Increased DMT1 but not IREG1 or HFE mRNA following iron depletion therapy in hereditary haemochromatosis Gut, August 1, 2004; 53(8): 1174 - 1179. [Abstract] [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020