The murine growth differentiation factor 15 is not essential for systemic iron homeostasis in phlebotomized mice

被引:88
作者
Casanovas, Guillem [1 ,2 ,3 ]
Spasic, Maja Vujic [1 ,2 ]
Casu, Carla [4 ]
Rivella, Stefano [4 ,5 ]
Strelau, Jens [6 ]
Unsicker, Klaus [7 ]
Muckenthaler, Martina U. [1 ,2 ]
机构
[1] Univ Heidelberg Hosp, Dept Pediat Oncol Hematol & Immunol, Heidelberg, Germany
[2] Mol Med Partnership Unit, Heidelberg, Germany
[3] European Mol Biol Lab, D-69012 Heidelberg, Germany
[4] WCMC, Dept Pediat, Div Hematol Oncol, New York, NY USA
[5] WCMC, Dept Cell & Dev Biol, New York, NY USA
[6] Interdisciplinary Ctr Neurosci IZN, Dept Neuroanat, Heidelberg, Germany
[7] Univ Freiburg, Dept Mol Embryol, Inst Anat & Cell Biol, D-79106 Freiburg, Germany
基金
美国国家卫生研究院;
关键词
TGF-BETA SUPERFAMILY; INEFFECTIVE ERYTHROPOIESIS; HEPCIDIN EXPRESSION; THALASSEMIA; CYTOKINE-1; GDF15; FERROPORTIN; METABOLISM; BINDING; RAT;
D O I
10.3324/haematol.2012.069807
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
In conditions of increased erythropoiesis, expression of hepcidin, the master regulator of systemic iron homeostasis, is decreased to allow for the release of iron into the blood stream from duodenal enterocytes and macrophages. It has been suggested that hepcidin suppression is controlled by growth differentiation factor 15 (GDF15), a member of the transforming growth factor-beta superfamily of cytokines that is secreted from developing erythroblasts. In this study, we analyzed iron-related parameters in mice deficient for GDF15 under steady-state conditions and in response to increased erythropoietic activity induced by blood loss. We demonstrate that GDF15 suppresses the hepatic mRNA expression of some BMP/TGF beta target genes but not of hepcidin, and show that GDF15 is not required to balance iron homeostasis in response to blood loss.
引用
收藏
页码:444 / 447
页数:4
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