|
|
Blood, 15 September 2005, Vol. 106, No. 6, pp. 2189-2195.
Prepublished online as a Blood First Edition Paper on May 24, 2005; DOI 10.1182/blood-2005-02-0629.
 Previous Article | Table of Contents | Next Article 
RED CELLS
Contribution of Hfe expression in macrophages to the regulation of hepatic hepcidin levels and iron loading
Hortence Makui,
Ricardo J. Soares,
Wenlei Jiang,
Marco Constante, and
Manuela M. Santos
From the Centre de recherche, Centre hospitalier de l'Université de Montréal (CHUM)-Hôpital Notre-Dame, Montréal, Québec, Canada; and UnIGENe, Instituto de Biologia Molecular e Celular, Porto, Portugal.
Hereditary hemochromatosis (HH), an iron overload disease associated with mutations in the HFE gene, is characterized by increased intestinal iron absorption and consequent deposition of excess iron, primarily in the liver. Patients with HH and Hfe-deficient (Hfe-/-) mice manifest inappropriate expression of the iron absorption regulator hepcidin, a peptide hormone produced by the liver in response to iron loading. In this study, we investigated the contribution of Hfe expression in macrophages to the regulation of liver hepcidin levels and iron loading. We used bone marrow transplantation to generate wild-type (wt) and Hfe-/- mice chimeric for macrophage Hfe gene expression. Reconstitution of Hfe-deficient mice with wt bone marrow resulted in augmented capacity of the spleen to store iron and in significantly decreased liver iron loading, accompanied by a significant increase of hepatic hepcidin mRNA levels. Conversely, wt mice reconstituted with Hfe-deficient bone marrow had a diminished capacity to store iron in the spleen but no significant alterations of liver iron stores or hepcidin mRNA levels. Our results suggest that macrophage Hfe participates in the regulation of splenic and liver iron concentrations and liver hepcidin expression. (Blood. 2005;106:2189-2195)
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
Related Article in Blood Online:
-
The iron sensor: macrophage, hepatocyte, both?
- Robert E. Fleming
Blood 2005 106: 1893-1894.
[Full Text]
[PDF]
This article has been cited by other articles:
|
|
|
|
 
H. Huang, M. Constante, A. Layoun, and M. M. Santos
Contribution of STAT3 and SMAD4 pathways to the regulation of hepcidin by opposing stimuli
Blood,
April 9, 2009;
113(15):
3593 - 3599.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. E. Fleming
Crypt cell hypothesis: technical knock-out
Blood,
May 15, 2007;
109(10):
4114 - 4115.
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Constante, D. Wang, V.-A. Raymond, M. Bilodeau, and M. M. Santos
Repression of Repulsive Guidance Molecule C during Inflammation Is Independent of Hfe and Involves Tumor Necrosis Factor-{alpha}
Am. J. Pathol.,
February 1, 2007;
170(2):
497 - 504.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Constante, W. Jiang, D. Wang, V.-A. Raymond, M. Bilodeau, and M. M. Santos
Distinct requirements for Hfe in basal and induced hepcidin levels in iron overload and inflammation
Am J Physiol Gastrointest Liver Physiol,
August 1, 2006;
291(2):
G229 - G237.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. M Yunker, J. S Parboosingh, H. E Conradson, P. Faris, P. J Bridge, J. Buithieu, L. M Title, F. Charbonneau, S. Verma, E. M Lonn, et al.
The effect of iron status on vascular health
Vascular Medicine,
May 1, 2006;
11(2):
85 - 91.
[Abstract]
[PDF]
|
|
|
|
|
|
|
R. E. Fleming and R. S. Britton
Iron Imports. VI. HFE and regulation of intestinal iron absorption
Am J Physiol Gastrointest Liver Physiol,
April 1, 2006;
290(4):
G590 - G594.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
