Expression of iron transport proteins divalent metal transporter-1, Ferroportin-1, HFE and transferrin receptor-1 in human monocyte-derived dendritic cells

2007 ◽  
Vol 25 (3) ◽  
pp. 287-296 ◽  
Author(s):  
Martin Brinkmann ◽  
Regina Teuffel ◽  
Nihay Laham ◽  
Rachel Ehrlich ◽  
Patrice Decker ◽  
...  
2001 ◽  
Vol 120 (6) ◽  
pp. 1412-1419 ◽  
Author(s):  
Heinz Zoller ◽  
Günter Weiss ◽  
Igor Theurl ◽  
Robert O. Koch ◽  
Wolfgang Vogel ◽  
...  

2000 ◽  
Vol 278 (6) ◽  
pp. G930-G936 ◽  
Author(s):  
Phillip S. Oates ◽  
Carla Thomas ◽  
Elizabeth Freitas ◽  
Matthew J. Callow ◽  
Evan H. Morgan

Regulation of iron absorption is thought to be mediated by the amount of iron taken up by duodenal crypt cells via the transferrin receptor (TfR)-transferrin cycle and the activity of the divalent metal transporter (DMT1), although DMT1 cannot be detected morphologically in crypt cells. We investigated the uptake of transferrin-bound iron by duodenal enterocytes in Wistar rats fed different levels of iron and Belgrade (b/b) rats in which iron uptake by the transferrin cycle is defective because of a mutation in DMT1. We showed that DMT1 in our colony of b/b rats contains the G185R mutation, which in enterocytes results in reduced cellular iron content and increased DMT1 gene expression similar to levels in iron deficiency of normal rats. In all groups the uptake of transferrin-bound iron by crypt cells was directly proportional to plasma iron concentration, being highest in iron-loaded Wistar rats and b/b rats. We conclude that the uptake of transferrin-bound iron by developing enterocytes is largely independent of DMT1.


Blood ◽  
2003 ◽  
Vol 101 (10) ◽  
pp. 4148-4154 ◽  
Author(s):  
Susanne Ludwiczek ◽  
Elmar Aigner ◽  
Igor Theurl ◽  
Günter Weiss

Abstract Under chronic inflammatory conditions cytokines induce a diversion of iron traffic, leading to hypoferremia and retention of the metal within the reticuloendothelial system. However, the regulatory pathways underlying these disturbances of iron homeostasis are poorly understood. We investigated transferrin receptor (TfR)–dependent and –independent iron transport mechanisms in cytokine-stimulated human monocytic cell lines THP-1 and U937. Combined treatment of cells with interferon-γ (IFN-γ) and lipopolysaccharide (LPS) reduced TfR mRNA levels, surface expression, and iron uptake, and these effects were reversed by interleukin-10 (IL-10), thus stimulating TfR-mediated iron acquisition. IFN-γ and LPS dose-dependently increased the cellular expression of divalent metal transporter-1, a transmembrane transporter of ferrous iron, and stimulated the uptake of nontransferrin bound iron (NTBI) into cells. At the same time, IFN-γ and LPS down-regulated the expression of ferroportin mRNA, a putative iron exporter, and decreased iron release from monocytes. Preincubation with IL-10 partly counteracted these effects. Our results demonstrate that the proinflammatory stimuli IFN-γ and LPS increase the uptake of NTBI via stimulation of divalent metal transporter-1 expression and cause retention of the metal within monocytes by down-regulating ferroportin synthesis. Opposite, the anti-inflammatory cytokine IL-10 stimulates TfR-mediated iron uptake into activated monocytes. The regulation of iron transport by cytokines is a key mechanism in the pathogenesis of anemia of chronic disease and a promising target for therapeutic intervention.


2001 ◽  
Vol 120 (5) ◽  
pp. A681
Author(s):  
Donatella Barisani ◽  
Antonina Parafioriti ◽  
Elisabetta Armiraglio ◽  
Dario Conte ◽  
Robert O. Koch ◽  
...  

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