Heart Ferroportin Protein Content Is Regulated by Heart Iron Concentration and Systemic Hepcidin Expression

The purpose of the study was to investigate the expression of ferroportin protein following treatments that affect systemic hepcidin. Administration of erythropoietin to C57BL/6J mice decreased systemic hepcidin expression; it also increased heart ferroportin protein content, determined by immunoblo...

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Published in:International journal of molecular sciences 2022-05, Vol.23 (11), p.5899
Main Authors: Berezovsky, Betty, Frýdlová, Jana, Gurieva, Iuliia, Rogalsky, Daniel W, Vokurka, Martin, Krijt, Jan
Format: Article
Language:English
Subjects:
Animals
Blood diseases
Cardiomyocytes
Cation Transport Proteins
Erythropoietin
Heart
Heart failure
Heme
Hepcidin
Hepcidins - genetics
Hepcidins - metabolism
Homeostasis
Iron
Iron - metabolism
Iron regulatory protein
Liver
Metabolism
Mice
Mice, Inbred C57BL
Nutrient deficiency
Proteins
Rats
Rats, Wistar
Regulation
Regulatory sequences
Spleen
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Summary:The purpose of the study was to investigate the expression of ferroportin protein following treatments that affect systemic hepcidin. Administration of erythropoietin to C57BL/6J mice decreased systemic hepcidin expression; it also increased heart ferroportin protein content, determined by immunoblot in the membrane fraction, to approximately 200% of control values. This increase in heart ferroportin protein is very probably caused by a decrease in systemic hepcidin expression, in accordance with the classical regulation of ferroportin by hepcidin. However, the control of heart ferroportin protein by systemic hepcidin could apparently be overridden by changes in heart non-heme iron content since injection of ferric carboxymaltose to mice at 300 mg Fe/kg resulted in an increase in liver hepcidin expression, heart non-heme iron content, and also a threefold increase in heart ferroportin protein content. In a separate experiment, feeding an iron-deficient diet to young Wistar rats dramatically decreased liver hepcidin expression, while heart non-heme iron content and heart ferroportin protein content decreased to 50% of controls. It is, therefore, suggested that heart ferroportin protein is regulated primarily by the iron regulatory protein/iron-responsive element system and that the regulation of heart ferroportin by the hepcidin-ferroportin axis plays a secondary role.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms23115899