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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Erythropoiesis-driven regulation of hepcidin in human red cell disorders is better reflected through concentrations of soluble transferrin receptor rather than growth differentiation factor 15

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Fertrin, Kleber Yotsumoto [1] ; Lanaro, Carolina [1] ; Franco-Penteado, Carla Fernanda [1] ; de Albuquerque, Dulcineia Martins [1] ; Bandeira de Mello, Mariana Rezende [1] ; Pallis, Flavia Rubia [1] ; Cavalcanti Bezerra, Marcos Andre [2] ; Domingues Hatzlhofer, Betania Lucena [3] ; Olbina, Gordana [4] ; Olalla Saad, Sara Terezinha [1] ; Araujo, Aderson da Silva [3] ; Westerman, Mark [4] ; Costa, Fernando Ferreira [1]
Total Authors: 13
Affiliation:
[1] Univ Estadual Campinas, Hematol & Hemotherapy Ctr, INCTS, Campinas, SP - Brazil
[2] Fed Univ Pernambuco UFPE, Ctr Biol Sci, Recife, PE - Brazil
[3] HEMOPE Hematol & Hemotherapy Ctr Pernambuco, Recife, PE - Brazil
[4] Intrins LifeSci LLC, La Jolla, CA - USA
Total Affiliations: 4
Document type: Journal article
Source: American Journal of Hematology; v. 89, n. 4, p. 385-390, APR 2014.
Web of Science Citations: 13
Abstract

Growth differentiation factor 15 (GDF-15) is a bone marrow-derived cytokine whose ability to suppress iron regulator hepcidin in vitro and increased concentrations found in patients with ineffective erythropoiesis (IE) suggest that hepcidin deficiency mediated by GDF-15 may be the pathophysiological explanation for nontransfusional iron overload. We aimed to compare GDF-15 production in anemic states with different types of erythropoietic dysfunction. Complete blood counts, biochemical markers of iron status, plasma hepcidin, GDF-15, and known hepcidin regulators {[}interleukin-6 and erythropoietin (EPO)] were measured in 87 patients with red cell disorders comprising IE and hemolytic states: thalassemia, sickle cell anemia, and cobalamin deficiency. Healthy volunteers were also evaluated for comparison. Neither overall increased EPO, nor variable GDF-15 concentrations correlated with circulating hepcidin concentrations (P = 0.265 and P = 0.872). Relative hepcidin deficiency was found in disorders presenting with concurrent elevation of GDF-15 and soluble transferrin receptor (sTfR), a biomarker of erythropoiesis, and sTfR had the strongest correlation with hepcidin (r(S) = -0.584, P < 0.0001). Our data show that high concentrations of GDF-15 in vivo are not necessarily associated with pathological hepcidin reduction, and hepcidin deficiency was only found when associated with sTfR overproduction. sTfR elevation may be a necessary common denominator of erythropoiesis-driven mechanisms to favor iron absorption in anemic states and appears a suitable target for investigative approaches to iron disorders. Am. J. Hematol. 89:385-390, 2014. (c) 2013 Wiley Periodicals, Inc. (AU)

FAPESP's process: 08/57441-0 - Clinical, cellular and molecular alterations in hemoglobinopathies and other hereditary hemolytic anemias
Grantee:Fernando Ferreira Costa
Support type: Research Projects - Thematic Grants