title: Identification of erythroferrone as an erythroid regulator of iron metabolism.
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.
authors.affiliation: Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.
authors.forename: Léon
authors.initials: L
authors.lastname: Kautz
authors.affiliation: Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.
authors.forename: Grace
authors.initials: G
authors.lastname: Jung
authors.affiliation: Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.
authors.forename: Erika V
authors.initials: EV
authors.lastname: Valore
authors.affiliation: 1] Department of Pediatrics, Division of Hematology-Oncology, Weill Cornell Medical College, New York, New York, USA. [2] Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, New York, USA.
authors.forename: Stefano
authors.initials: S
authors.lastname: Rivella
authors.affiliation: Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.
authors.forename: Elizabeta
authors.initials: E
authors.lastname: Nemeth
authors.affiliation: 1] Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA. [2] Department of Pathology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.
authors.forename: Tomas
authors.initials: T
authors.lastname: Ganz
mesh_terms: D000740:Anemia / Q000209:etiology / Q000378:metabolism; D000818:Animals; D015153:Blotting, Western; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D000068817:Epoetin Alfa; D004920:Erythropoiesis / Q000187:drug effects* / Q000502:physiology; D004921:Erythropoietin / Q000378:metabolism; D020869:Gene Expression Profiling; D006454:Hemoglobins / Q000378:metabolism*; D006470:Hemorrhage / Q000150:complications / Q000378:metabolism; D064451:Hepcidins / Q000378:metabolism*; D006728:Hormones / Q000494:pharmacology*; D007501:Iron / Q000378:metabolism*; D019190:Iron Overload / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D011994:Recombinant Proteins / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017086:beta-Thalassemia / Q000378:metabolism* / Q000473:pathology
chemical_list: D006454:Hemoglobins; D064451:Hepcidins; D006728:Hormones; D012333:RNA, Messenger; D011994:Recombinant Proteins; D004921:Erythropoietin; D000068817:Epoetin Alfa; D007501:Iron