Vitamin D effects on cell proliferation and gene expression profile of breast canc...
| Full text | |
| Author(s): Show less - |
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 |