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Blood, 1 April 2006, Vol. 107, No. 7, pp. 2702-2704. Prepublished online as a Blood First Edition Paper on December 6, 2005; DOI 10.1182/blood-2005-07-2854. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-07-2854v1 107/7/2702    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 Dallalio, G. Articles by Means, R. T. Search for Related Content PubMed PubMed Citation Articles by Dallalio, G. Articles by Means, R. T., Jr Related Collections Hematopoiesis and Stem Cells Red Cells Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Brief report Hepcidin inhibits in vitro erythroid colony formation at reduced erythropoietin concentrations Gail Dallalio, Erin Law, and Robert T. Means, Jr From the Medical and Research Services, Lexington Department of Veterans Affairs Medical Center and the Hematology/Oncology Division/Markey Cancer Center, University of Kentucky College of Medicine, Lexington. The anemia of chronic disease (ACD) results from 3 major processes: slightly shortened red cell survival, impaired reticuloendothelial system iron mobilization, and impaired erythropoiesis. Hepcidin is an acute-phase protein with specific iron regulatory properties, which, along with the anemia seen with increased hepcidin expression, have led many to consider it the major mediator of ACD. However, if hepcidin is the major factor responsible for ACD, then it should also contribute to the impaired erythropoiesis observed in this syndrome. Erythroid colony formation in vitro was inhibited by hepcidin at erythropoietin (Epo) concentrations less than or equal to 0.5 U/mL but not at Epo 1.0 U/mL. At Epo concentrations of 0.3 U/mL, HCD57 erythroleukemia cells exposed to hepcidin exhibit decreased expression of the antiapoptotic protein pBad compared with controls. These studies suggest that hepcidin may contribute to anemia in ACD not only through effects on iron metabolism, but also through inhibition of erythroid progenitor proliferation and survival. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Sharma, E. Nemeth, Y.-H. Chen, J. Goodnough, A. Huston, G.D. Roodman, T. Ganz, and A. Lichtenstein Involvement of Hepcidin in the Anemia of Multiple Myeloma Clin. Cancer Res., June 1, 2008; 14(11): 3262 - 3267. [Abstract] [Full Text] [PDF] D. W. Swinkels and J. F. M. Wetzels Hepcidin: a new tool in the management of anaemia in patients with chronic kidney disease? Nephrol. Dial. Transplant., May 21, 2008; (2008) gfn267v1. [Full Text] [PDF] C. N. Roy, H. H. Mak, I. Akpan, G. Losyev, D. Zurakowski, and N. C. Andrews Hepcidin antimicrobial peptide transgenic mice exhibit features of the anemia of inflammation Blood, May 1, 2007; 109(9): 4038 - 4044. [Abstract] [Full Text] [PDF] D. Yoon, Y. D. Pastore, V. Divoky, E. Liu, A. E. Mlodnicka, K. Rainey, P. Ponka, G. L. Semenza, A. Schumacher, and J. T. Prchal Hypoxia-inducible Factor-1 Deficiency Results in Dysregulated Erythropoiesis Signaling and Iron Homeostasis in Mouse Development J. Biol. Chem., September 1, 2006; 281(35): 25703 - 25711. [Abstract] [Full Text] [PDF] J. Truksa, H. Peng, P. Lee, and E. Beutler Bone morphogenetic proteins 2, 4, and 9 stimulate murine hepcidin 1 expression independently of Hfe, transferrin receptor 2 (Tfr2), and IL-6 PNAS, July 5, 2006; 103(27): 10289 - 10293. [Abstract] [Full Text] [PDF]

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