Expression of transferrin receptor 2 in normal and neoplastic hematopoietic cells

Kawabata, Hiroshi; Nakamaki, Tsuyoshi; Ikonomi, Pranvera; Smith, Richard; Germain, Rasha; Koeffler, H. Phillip

doi:10.1182/blood.v98.9.2714

Cited by 108 publications

(100 citation statements)

References 19 publications

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“…Previous studies have suggested that TFR2 is expressed in erythroid cells [14] and is regulated by erythroid-specific transcription factors in vivo [15]. GWAS have suggested a correlation between the TFR2 genomic region and various hematological traits [16][17][18][19].…”

Section: Discussionmentioning

confidence: 99%

“…In addition to the liver, Tfr2 expression was also detected in the BM and early erythroid progenitors [14] with expression decreasing with cell differentiation [14]. Real-time PCR analysis revealed that Tfr2 expression begins between day 8 and 11 of embryonic development, which coincides with the time when primary hematopoietic cells move from the yolk sac to the liver for initial hematopoiesis [15].…”

Section: Introductionmentioning

confidence: 99%

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Hematopoietic deletion of transferrin receptor 2 in mice leads to a block in erythroid differentiation during iron‐deficient anemia

et al. 2016

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Iron metabolism and erythropoiesis are inherently interlinked physiological processes. Regulation of iron metabolism is mediated by the iron-regulatory hormone hepcidin. Hepcidin limits the amount of iron released into the blood by binding to and causing the internalization of the iron exporter, ferroportin. A number of molecules and physiological stimuli, including erythropoiesis, are known to regulate hepcidin. An increase in erythropoietic demand decreases hepcidin, resulting in increased bioavailable iron in the blood. Transferrin receptor 2 (TFR2) is involved in the systemic regulation of iron metabolism. Patients and mice with mutations in TFR2 develop hemochromatosis due to inappropriate hepcidin levels relative to body iron. Recent studies from our laboratory and others have suggested an additional role for TFR2 in response to iron-restricted erythropoiesis. These studies used mouse models with perturbed systemic iron metabolism: anemic mice lacking matriptase-2 and Tfr2, or bone marrow transplants from iron-loaded Tfr2 null mice. We developed a novel transgenic mouse model which lacks Tfr2 in the hematopoietic compartment, enabling the delineation of the role of Tfr2 in erythroid development without interfering with its role in systemic iron metabolism. We show that in the absence of hematopoietic Tfr2 immature polychromatic erythroblasts accumulate with a concordant reduction in the percentage of mature erythroid cells in the spleen and bone marrow of anemic mice. These results demonstrate that erythroid Tfr2 is essential for an appropriate erythropoietic response in iron-deficient anemia. These findings may be of relevance in clinical situations in which an immediate and efficient erythropoietic response is required.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hematopoietic deletion of transferrin receptor 2 in mice leads to a block in erythroid differentiation during iron‐deficient anemia

et al. 2016

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“…TfR2 is highly expressed in the liver (22). There is some evidence that it is expressed in early erythroid precursor cells (21); however, this is controversial (1). Our recent studies (35) suggest that liver-expressed TfR2 plays a predominant role in the regulation of iron metabolism.…”

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confidence: 97%

Defective trafficking and localization of mutated transferrin receptor 2: implications for type 3 hereditary hemochromatosis

Wallace¹,

Summerville²,

Crampton³

et al. 2008

American Journal of Physiology-Cell Physiology

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“…15 As a further level of complexity, the TFR2 gene, which has two consensus sequences for the erythroid transcription factor GATA-1 in its promoter, 12 is expressed in immature erythroid cells 16 where it is a component of the erythropoietin receptor (EPOR) complex. 17 The TFR2-EPOR association is required for the efficient transport of EPOR to the cell surface.…”

mentioning

confidence: 99%

Regulation of cell surface transferrin receptor-2 by iron-dependent cleavage and release of a soluble form

et al. 2015

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Expression of transferrin receptor 2 in normal and neoplastic hematopoietic cells

Cited by 108 publications

References 19 publications

Hematopoietic deletion of transferrin receptor 2 in mice leads to a block in erythroid differentiation during iron‐deficient anemia

Hematopoietic deletion of transferrin receptor 2 in mice leads to a block in erythroid differentiation during iron‐deficient anemia

Defective trafficking and localization of mutated transferrin receptor 2: implications for type 3 hereditary hemochromatosis

Regulation of cell surface transferrin receptor-2 by iron-dependent cleavage and release of a soluble form

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