Please use this identifier to cite or link to this item: http://hdl.handle.net/10216/108247
Author(s): Neves, JV
Caldas, C
Ramos, M
Rodrigues, PN
Title: Hepcidin-dependent regulation of erythropoiesis during anemia in a teleost fish, dicentrarchus labrax
Publisher: Public Library of Science
Issue Date: 2016
Abstract: Anemia is a common disorder, characterized by abnormally low levels of red blood cells or hemoglobin. The mechanisms of anemia development and response have been thoroughly studied in mammals, but little is known in other vertebrates, particularly teleost fish. In this study, different degrees of anemia were induced in healthy European sea bass specimens (Dicentrarchus labrax) and at pre-determined time points hematological parameters, liver iron content and the expression of genes involved in iron homeostasis and hematopoiesis, with particular attention on hepcidins, were evaluated. The experimental anemia prompted a decrease in hamp1 expression in all tested organs, in accordance to an increased need for iron absorption and mobilization, with slight increases in hamp2 in the kidney and intestine. The liver was clearly the major organ involved in iron homeostasis, decreasing its iron content and showing a gene expression profile consistent with an increased iron release and mobilization. Although both the spleen and head kidney are involved in erythropoiesis, the spleen was found to assume a more preponderant role in the recovery of erythrocyte levels. The intestine was also involved in the response to anemia, through the increase of iron transporting genes. Administration of Hamp1 or Hamp2 mature peptides showed that only Hamp1 affects hematological parameters and liver iron content. In conclusion, the molecular mechanisms of response to anemia present in sea bass are similar to the ones described for mammals, with these results indicating that the two hepcidin types from teleosts assume different roles during anemia.
Subject: Iron-metabolism
Transcription factors
Mitochondrial heme
Peptide hepcidin
Expression
Gene
Overload
Liver
BMP6
Inflammation
URI: http://hdl.handle.net/10216/108247
Source: PLoS ONE, vol. 11 (4):e0153940
Related Information: info:eu-repo/grantAgreement/FCT/SFRH/SFRH/BPD/86380/2012/PT
Document Type: Artigo em Revista Científica Internacional
Rights: openAccess
License: http://creativecommons.org/licenses/by/4.0/
Appears in Collections:I3S - Artigo em Revista Científica Internacional

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