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Constitutive Hepcidin Expression Prevents Iron Overload in a Mouse Model of Hemochromatosis by Gaël Nicolas; Lydie Viatte; Dan-Qing Lou; Myriam Bennoun; Carole Beaumont; Axel Kahn; Nancy C. Andrews; Sophie Vaulont is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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Hereditary hemochromatosis is a prevalent genetic disorder of iron hyperabsorption leading to hyperferremia, tissue iron deposition and complications including cirrhosis, hepatocarcinoma, cardiomyopathy and diabetes. Most individuals affected with hereditary hemochromatosis are homozygous with respect to a missense mutation that disrupts the conformation of HFE, an atypical HLA class I molecule (ref. 1; OMIM 235200). Mice lacking Hfe or producing a C282Y mutant Hfe protein develop hyperferremia and have high hepatic iron levels. In both humans and mice, hereditary hemochromatosis is associated with a paucity of iron in reticuloendothelial cells. It has been suggested that HFE modulates uptake of transferrin-bound iron by undifferentiated intestinal crypt cells, thereby programming the absorptive capacity of enterocytes derived from these cells; however, this model is unproven and controversial. Hepcidin, a peptide hormone (HAMP; OMIM 606464), seems to act in the same regulatory pathway as HFE. Although expression of mouse Hamp is normally greater during iron overload, Hfe-/- mice have inappropriately low expression of Hamp. We crossed Hfe-/- mice with transgenic mice overexpressing

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Author

Gaël Nicolas; Lydie Viatte; Dan-Qing Lou; Myriam Bennoun; Carole Beaumont; Axel Kahn; Nancy C. Andrews; Sophie Vaulont

Publisher

Springer Science and Business Media LLC

Published

2003

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)