Hepcidin mRNA levels in mouse liver respond to inhibition of erythropoiesis
Language English Country Czech Republic Media print
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
16497104
DOI
10.33549/physiolres.930841
PII: 841
Knihovny.cz E-resources
- MeSH
- Time Factors MeSH
- Erythropoietin pharmacology MeSH
- Erythropoiesis * drug effects radiation effects MeSH
- Phenylhydrazines MeSH
- Ferritins metabolism MeSH
- Ferroportin MeSH
- GPI-Linked Proteins MeSH
- Anemia, Hemolytic chemically induced metabolism physiopathology MeSH
- Hemolysis * drug effects radiation effects MeSH
- Hepcidins MeSH
- Liver drug effects metabolism radiation effects MeSH
- Antimicrobial Cationic Peptides metabolism MeSH
- Membrane Proteins metabolism MeSH
- RNA, Messenger metabolism MeSH
- Mice, Inbred C57BL MeSH
- Mice MeSH
- Polycythemia metabolism physiopathology MeSH
- Reverse Transcriptase Polymerase Chain Reaction MeSH
- Hemochromatosis Protein MeSH
- Cation Transport Proteins metabolism MeSH
- Receptors, Transferrin metabolism MeSH
- Gene Expression Regulation MeSH
- Iron Compounds metabolism MeSH
- Gamma Rays MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- Erythropoietin MeSH
- Phenylhydrazines MeSH
- Ferritins MeSH
- Ferroportin MeSH
- GPI-Linked Proteins MeSH
- Hamp protein, mouse MeSH Browser
- Hepcidins MeSH
- HJV protein, mouse MeSH Browser
- Antimicrobial Cationic Peptides MeSH
- Membrane Proteins MeSH
- RNA, Messenger MeSH
- phenylhydrazine MeSH Browser
- Hemochromatosis Protein MeSH
- Cation Transport Proteins MeSH
- Receptors, Transferrin MeSH
- Iron Compounds MeSH
- solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2 MeSH Browser
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.
References provided by Crossref.org
Effect of Erythropoietin on the Expression of Murine Transferrin Receptor 2
Matriptase-2 and Hemojuvelin in Hepcidin Regulation: In Vivo Immunoblot Studies in Mask Mice
Effect of iron overload and iron deficiency on liver hemojuvelin protein
