Abstract
Recovery from blood loss requires a greatly enhanced supply of iron to support expanded erythropoiesis. After hemorrhage, suppression of the iron-regulatory hormone hepcidin allows increased iron absorption and mobilization from stores. We identified a new hormone, erythroferrone (ERFE), that mediates hepcidin suppression during stress erythropoiesis. ERFE is produced by erythroblasts in response to erythropoietin. ERFE-deficient mice fail to suppress hepcidin rapidly after hemorrhage and exhibit a delay in recovery from blood loss. ERFE expression is greatly increased in Hbb(th3/+) mice with thalassemia intermedia, where it contributes to the suppression of hepcidin and the systemic iron overload characteristic of this disease.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Anemia / etiology
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Anemia / metabolism
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Animals
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Blotting, Western
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Disease Models, Animal
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Enzyme-Linked Immunosorbent Assay
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Epoetin Alfa
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Erythropoiesis / drug effects*
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Erythropoiesis / physiology
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Erythropoietin / metabolism
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Gene Expression Profiling
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Hemoglobins / metabolism*
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Hemorrhage / complications
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Hemorrhage / metabolism
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Hepcidins / metabolism*
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Hormones / pharmacology*
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Iron / metabolism*
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Iron Overload / drug therapy*
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Iron Overload / metabolism
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Iron Overload / pathology
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Liver / metabolism
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Liver / pathology
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Molecular Sequence Data
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RNA, Messenger / genetics
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Real-Time Polymerase Chain Reaction
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Recombinant Proteins / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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beta-Thalassemia / metabolism*
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beta-Thalassemia / pathology
Substances
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Hemoglobins
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Hepcidins
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Hormones
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RNA, Messenger
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Recombinant Proteins
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Erythropoietin
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Epoetin Alfa
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Iron
Associated data
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GENBANK/KF984314
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GEO/GSE52740