Ferroportin1: a new iron export molecule?

Le, Nghia T.V.; Richardson, Des R.

doi:10.1016/s1357-2725(01)00104-2

Cited by 35 publications

(22 citation statements)

References 13 publications

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“…Based on such studies, some chelators such as CPX may not be suited for the treatment of cancer in vivo but could possibly be used to increase angiogenesis for wound healing [174]. Indeed, the chelator-mediated response obtained, that is, either angiogenesis or anti-proliferative activity, may be dependent on the extent of Fe chelation and the intracellular pathways targeted by these ligands [85,175,176]. Indeed, these competing pathways can be induced by Fe chelation and it may be possible to pharmacologically promote either pathway depending upon ligand design [176].…”

Section: Potent Iron Chelators Overwhelm the Pro-angiogenic And Cell mentioning

confidence: 99%

“…While Fe chelation increases VEGF-1 expression that promotes angiogenesis [174,175], it must be pointed out that there are also counteracting pathways induced by Fedepletion which cause cell cycle arrest and apoptosis by interfering with the activity and expression of a variety of molecular targets such as Ndrg1 [85], ribonucleotide reductase [109], cyclin D1 [98], cdk2 [98], and p21 CIP1/WAF1 [98,144] (see Table 4). The multiple mechanisms by which potent Fe chelators cause cell cycle arrest and programmed cell death may overwhelm the angiogenic effects of VEGF-1 and account for the anti-tumor activity of chelators in vivo [176].…”

Section: Potent Iron Chelators Overwhelm the Pro-angiogenic And Cell mentioning

confidence: 99%

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Molecular Mechanisms of Iron Uptake by Cells and the Use of Iron Chelators for the Treatment of Cancer

Richardson

2005

CMC

116

102

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The field of iron (Fe) metabolism has been invigorated in the past 10 years with the discovery of a variety of new molecules involved in the homeostatic control of this critical nutrient. These proteins include the transferrin receptor 2, frataxin, hephaestin, hepcidin, hemojuvelin and others. Basic understanding of the metabolism of Fe in cells is vital in order to develop Fe chelators for the treatment of a variety of disease states. In addition, examination of the role of Fe in the regulation of cell cycle progression and angiogenesis has led to investigations of the use of novel Fe chelators as anti-proliferative agents. These studies have resulted in the identification of new ligands that show selective and potent anti-tumor activity in vitro and in vivo. Moreover, the ability of these chelators to inhibit growth is not only limited to the inhibition of DNA synthesis. In fact, there is a range of targets that are affected by Fe-depletion, such as molecules involved in cell cycle control, angiogenesis and metastasis suppression. These include hypoxia-inducible factor-1 alpha (HIF-1 alpha), vascular endothelial growth factor-1 (VEGF1), p21(CIP1/WAF1), cyclin D1 and the protein product of the N-myc downstream regulated gene-1 (Ndrg1). As such, Fe chelators can now be designed to target molecules to induce specific effects, for instance, angiogenesis or metastasis suppression.

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Section: Potent Iron Chelators Overwhelm the Pro-angiogenic And Cell mentioning

confidence: 99%

Section: Potent Iron Chelators Overwhelm the Pro-angiogenic And Cell mentioning

confidence: 99%

Molecular Mechanisms of Iron Uptake by Cells and the Use of Iron Chelators for the Treatment of Cancer

Richardson

2005

CMC

116

102

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“…Hepcidin is induced during infections and inflammation and then acts by binding to ferroportin, which is an iron exporter present on the absorptive surface of duodenal enterocytes, macrophages, and hepatocytes [8]. After hepcidin and ferroportin interact, ferroportin is internalized and degraded, consequently leading to intracellular iron sequestration and decreased iron absorption [9].…”

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confidence: 99%

Inflammation-Induced Hepcidin is Associated with the Development of Anemia and Coronary Artery Lesions in Kawasaki Disease

Kuo

Yang

Chuang³

et al. 2012

J Clin Immunol

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“…Iron in the intestinal lumen is firstly reduced by duodenal cytochrome b (Dcytb, a ferric reductase) and then transported across the apical membrane of intestinal cells by DMT1 (divalent metal transporter) [Andrews, 2000]. Once inside the cells, iron can either be stored in ferritin or transported across the basolateral membrane by ferroportin1 [Kaplan and Kushner, 2000;Le and Richardson, 2002]. The form of iron that is exported by ferroportin1 might be Fe 2+ .…”

Section: Discussionmentioning

confidence: 99%

“…The form of iron that is exported by ferroportin1 might be Fe 2+ . Ferroportin1 may work with hephaestin (or ceruoplasmin in other cell types), a ferroxidase, to load iron (Fe 3+ ) onto transferrin [Kaplan and Kushner, 2000;Le and Richardson, 2002]. The process of iron transport across the bloodbrain barrier (BBB) cells is very similar to that of iron transport across the cells lining the gut [Qian and Shen, 2001].…”

Section: Discussionmentioning

confidence: 99%

Distribution of Ferroportin1 Protein in Different Regions of Developing Rat Brain

Jiang

Cheng

et al. 2002

Dev Neurosci

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Ferroportin1 is a newly discovered transmembrane iron export protein. It plays a key role in Fe²⁺ transport across the basal membrane of enterocytes in the gut. It has been suggested that this protein might have the same role in Fe²⁺ transport across the abluminal membrane of the blood-brain barrier as it works in enterocytes. However, the presence of ferroportin1 in the brain has not been well determined. In the present study, we investigated expression of ferroportin1 protein in different brain regions, including cortex, hippocampus, striatum and substantia nigra, in developing male Sprague-Dawley rats. The results provided direct evidence for the existence of ferroportin1 protein in the rat brain. All brain areas examined have the ability to synthesize ferroportin1 protein. The findings also showed that age has a significant effect on the expression of ferroportin1 protein in the cortex, hippocampus, striatum and substantia nigra of the rat brain.

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Ferroportin1: a new iron export molecule?

Cited by 35 publications

References 13 publications

Molecular Mechanisms of Iron Uptake by Cells and the Use of Iron Chelators for the Treatment of Cancer

Molecular Mechanisms of Iron Uptake by Cells and the Use of Iron Chelators for the Treatment of Cancer

Inflammation-Induced Hepcidin is Associated with the Development of Anemia and Coronary Artery Lesions in Kawasaki Disease

Distribution of Ferroportin1 Protein in Different Regions of Developing Rat Brain

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