Hepcidin expression does not rescue the iron-poor phenotype of Kupffer cells in Hfe-null mice after liver transplantation.

@article{Garuti2010HepcidinED,
  title={Hepcidin expression does not rescue the iron-poor phenotype of Kupffer cells in Hfe-null mice after liver transplantation.},
  author={Cinzia Garuti and Yinghua Tian and Giuliana Montosi and Manuela Sabelli and Elena Corradini and Rolf E. Graf and Paolo Ventura and Alberto Vegetti and Pierre-Alain Clavien and Antonello Pietrangelo},
  journal={Gastroenterology},
  year={2010},
  volume={139 1},
  pages={315-22.e1}
}
BACKGROUND & AIMS Hemochromatosis is a common hereditary disease caused by mutations in HFE and characterized by increased absorption of iron in the intestine. However, the intestine does not appear to be the site of mutant HFE activity in the disease; we investigated the role of the liver-the source of the iron regulatory hormone hepcidin-in pathogenesis in mice. METHODS We exchanged livers between Hfe wild-type (+/+) and Hfe null (-/-) mice by orthotopic liver transplantation (OLT) and… CONTINUE READING

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