| First Author | Viatte L | Year | 2005 |
| Journal | Blood | Volume | 105 |
| Issue | 12 | Pages | 4861-4 |
| PubMed ID | 15713792 | Mgi Jnum | J:105053 |
| Mgi Id | MGI:3613344 | Doi | 10.1182/blood-2004-12-4608 |
| Citation | Viatte L, et al. (2005) Deregulation of proteins involved in iron metabolism in hepcidin-deficient mice. Blood 105(12):4861-4 |
| abstractText | Evidence is accumulating that hepcidin, a liver regulatory peptide, could be the common pathogenetic denominator of all forms of iron overload syndromes including HFE-related hemochromatosis, the most prevalent genetic disorder characterized by inappropriate iron absorption. To understand the mechanisms whereby hepcidin controls iron homeostasis in vivo, we have analyzed the level of iron-related proteins by Western blot and immunohistochemistry in hepcidin-deficient mice, a mouse model of severe hemochromatosis. These mice showed important increased levels of duodenal cytochrome b (Dcytb), divalent metal transporter 1 (DMT1), and ferroportin compared with control mice. Interestingly, the level of ferroportin was coordinately up-regulated in the duodenum, the spleen, and the liver (predominantly in the Kupffer cells). Finally, we also evidenced a decrease of ceruloplasmin in the liver of hepcidin-deficient mice. We hypothesized that the deregulation of these proteins might be central in the pathogenesis of iron overload, providing key therapeutic targets for iron disorders. |
