| Hepcidin mRNA levels in mouse liver respond to inhibition of erythropoiesis. | |
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MedLine Citation:
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PMID: 16497104 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hepcidin, a key regulator of iron metabolism, decreases intestinal absorption of iron and its release from macrophages. Iron, anemia, hypoxia, and inflammation were reported to influence hepcidin expression. To investigate regulation of the expression of hepcidin and other iron-related genes, we manipulated erythropoietic activity in mice. Erythropoiesis was inhibited by irradiation or posttransfusion polycythemia and stimulated by phenylhydrazine administration and erythropoietin. Gene expression of hepcidin and other iron-related genes (hemojuvelin, DMT1, ferroportin, transferrin receptors, ferritin) in the liver was measured by the real-time polymerase chain reaction. Hepcidin expression increased despite severe anemia when hematopoiesis was inhibited by irradiation. Suppression of erythropoiesis by posttransfusion polycythemia or irradiation also increased hepcidin mRNA levels. Compensated hemolysis induced by repeated phenylhydrazine administration did not change hepcidin expression. The decrease caused by exogenous erythropoeitin was blocked by postirradiation bone marrow suppression. The hemolysis and anemia decrease hepcidin expression only when erythropoiesis is functional; on the other hand, if erythropoiesis is blocked, even severe anemia does not lead to a decrease of hepcidin expression, which is indeed increased. We propose that hepcidin is exclusively sensitive to iron utilization for erythropoiesis and hepatocyte iron balance, and these changes are not sensed by other genes involved in the control of iron metabolism in the liver. |
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Authors:
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M Vokurka; J Krijt; K Sulc; E Necas |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Physiological research / Academia Scientiarum Bohemoslovaca Volume: 55 ISSN: 0862-8408 ISO Abbreviation: Physiol Res Publication Date: 2006 |
Date Detail:
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Created Date: 2006-12-20 Completed Date: 2007-02-15 Revised Date: 2008-04-02 |
Medline Journal Info:
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Nlm Unique ID: 9112413 Medline TA: Physiol Res Country: Czech Republic |
Other Details:
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Languages: eng Pagination: 667-74 Citation Subset: IM |
Affiliation:
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Institute of Pathophysiology, First Faculty of Medicine, Charles University, Prague, Czech Republic. mvoku@LF1.cuni.cz |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Anemia, Hemolytic
/
chemically induced,
metabolism,
physiopathology Animals Antimicrobial Cationic Peptides / metabolism* Cation Transport Proteins / metabolism Erythropoiesis* / drug effects, radiation effects Erythropoietin / pharmacology Ferritins / metabolism Gamma Rays Gene Expression Regulation Hemolysis* / drug effects, radiation effects Iron Compounds / metabolism Liver / drug effects, metabolism*, radiation effects Male Membrane Proteins / metabolism Mice Mice, Inbred C57BL Phenylhydrazines Polycythemia / metabolism, physiopathology RNA, Messenger / metabolism* Receptors, Transferrin / metabolism Reverse Transcriptase Polymerase Chain Reaction Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Antimicrobial Cationic Peptides; 0/Cation Transport Proteins; 0/Hfe2 protein, mouse; 0/Iron Compounds; 0/Membrane Proteins; 0/Phenylhydrazines; 0/RNA, Messenger; 0/Receptors, Transferrin; 0/hepcidin; 0/metal transporting protein 1; 0/solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2; 100-63-0/phenylhydrazine; 11096-26-7/Erythropoietin; 9007-73-2/Ferritins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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