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

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...

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Main Authors: Casanovas, Guillem (Author) , Spasić Vujić, Maja (Author) , Casu, Carla (Author) , Rivella, Stefano (Author) , Strelau, Jens (Author) , Unsicker, Klaus (Author) , Muckenthaler, Martina (Author)
Format: Article (Journal)
Language:English
Published: 2013
In: Haematologica, the hematology journal
Year: 2013, Volume: 98, Issue: 3, Pages: 444-447
ISSN:1592-8721
DOI:10.3324/haematol.2012.069807
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.3324/haematol.2012.069807
Verlag, lizenzpflichtig, Volltext: https://haematologica.org/article/view/6599
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Author Notes:Guillem Casanovas, Maja Vujić Spasić, Carla Casu, Stefano Rivella, Jens Strelau, Klaus Unsicker, and Martina U. Muckenthaler
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Summary: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-β 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/TGFβ target genes but not of hepcidin, and show that GDF15 is not required to balance iron homeostasis in response to blood loss.
Item Description:Gesehen am 12.03.2021
Physical Description:Online Resource
ISSN:1592-8721
DOI:10.3324/haematol.2012.069807

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