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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.
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Submitted July 18, 2005
Accepted November 20, 2005
Hepcidin inhibits in vitro erythroid colony formation at reduced erythropoietin concentrations
Gail Dallalio, Erin Law, and Robert T Means Jr*
Medical and Research Services, Lexington Department of Veterans Affairs Medical Center, Lexington, KY, USA; Hematology/Oncology Division/Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, USA
Medical and Research Services, Lexington Department of Veterans Affairs Medical Center, Lexington, KY, USA
* Corresponding author; email: robert.means{at}uky.edu.
The anemia of chronic disease (ACD) results from three 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 Epo concentrations  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 anti-apoptotic protein pBad compared to 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.
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