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Deficiency of the BMP Type I receptor ALK3 partly protects mice from anemia of inflammation

Overview of attention for article published in BMC Physiology, February 2018
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Title
Deficiency of the BMP Type I receptor ALK3 partly protects mice from anemia of inflammation
Published in
BMC Physiology, February 2018
DOI 10.1186/s12899-018-0037-z
Pubmed ID
Authors

Inka Gallitz, Niklas Lofruthe, Lisa Traeger, Nicole Bäumer, Verena Hoerr, Cornelius Faber, Tanja Kuhlmann, Carsten Müller-Tidow, Andrea U. Steinbicker

Abstract

Inflammatory stimuli induce the hepatic iron regulatory hormone hepcidin, which contributes to anaemia of inflammation (AI). Hepcidin expression is regulated by the bone morphogenetic protein (BMP) and the interleukin-6 (IL-6) signalling pathways. Prior results indicate that the BMP type I receptor ALK3 is mainly involved in the acute inflammatory hepcidin induction four and 72 h after IL-6 administration. In this study, the role of ALK3 in a chronic model of inflammation was investigated. The intact, heat-killed bacterium Brucella abortus (BA) was used to analyse its effect on the development of inflammation and hypoferremia in mice with hepatocyte-specific Alk3-deficiency (Alk3fl/fl; Alb-Cre) compared to control (Alk3fl/fl) mice. An iron restricted diet prevented development of the iron overload phenotype in mice with hepatocyte-specific Alk3 deficiency. Regular diet leads to iron overload and increased haemoglobin levels in these mice, which protects from the development of AI per se. Fourteen days after BA injection Alk3fl/fl; Alb-Cre mice presented milder anaemia (Hb 16.7 g/dl to 11.6 g/dl) compared to Alk3fl/fl control mice (Hb 14.9 g/dl to 8.6 g/dl). BA injection led to an intact inflammatory response in all groups of mice. In Alk3fl/fl; Alb-Cre mice, SMAD1/5/8 phosphorylation was reduced after BA as well as after infection with Staphylococcus aureus. The reduction of the SMAD1/5/8 signalling pathway due to hepatocyte-specific Alk3 deficiency partly suppressed the induction of STAT3 signalling. The results reveal in vivo, that 1) hepatocyte-specific Alk3 deficiency partly protects from AI, 2) the development of hypoferremia is partly dependent on ALK3, and 3) the ALK3/BMP/hepcidin axis may serve as a possible therapeutic target to attenuate AI.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 42 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 42 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 7 17%
Student > Master 4 10%
Student > Ph. D. Student 3 7%
Student > Bachelor 2 5%
Other 2 5%
Other 4 10%
Unknown 20 48%
Readers by discipline Count As %
Pharmacology, Toxicology and Pharmaceutical Science 6 14%
Biochemistry, Genetics and Molecular Biology 4 10%
Medicine and Dentistry 2 5%
Nursing and Health Professions 1 2%
Agricultural and Biological Sciences 1 2%
Other 5 12%
Unknown 23 55%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 16 August 2018.
All research outputs
#20,530,891
of 23,100,534 outputs
Outputs from BMC Physiology
#72
of 87 outputs
Outputs of similar age
#292,009
of 330,232 outputs
Outputs of similar age from BMC Physiology
#3
of 3 outputs
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