Relationship between Soluble Transferrin Receptors in Serum and Membrane-Bound Transferrin Receptors

Abstract

The expression of transferrin receptors on the cell membrane of erythroblasts was analysed with flow cytometry in patients with different forms of anaemia. At the same time the concentration of soluble transferrin receptors (sTfRs) was analysed in serum. It was shown that only in iron deficiency a high concentration of sTfRs in serum could be explained with an increased expression of transferrin receptors on the erythroblastic membrane. In anaemia of chronic disease and myelodysplasia a discrepancy between a low expression on the cell membrane and normal or elevated serum values was seen. From this study we conclude that the concentration of sTfRs in serum does not only depend on the expression of transferrin receptors on the erythroblasts but also on the erythroid activity.

Malarial anemia leads to adequately increased erythropoiesis in asymptomatic Kenyan children

“…48 Fourth, expression of transferrin receptors on individual erythroblasts is increased in iron deficiency but decreased in anemia of chronic disease. 18,49,50 If our assumption were true that also asymptomatic malaria does not lead to iron sequestration, then this would suggest that the increased serum transferrin receptor concentrations observed in children with malarial infection in our study are primarily due to increased erythropoiesis.…”

Soluble Transferrin Receptor and Its Ratio to Erythroblasts in Bone Marrow May Be a New Diagnostic Tool to Distinguish between Aplastic and Refractory Anemia

“…Kuiper-Kramer et al [11]reported that normal levels of serum sTfR were found in the sera of some MDS patients, whereas on the erythroid cell membrane the concentration of sTfR was reduced in a flow cytometric analysis using a double staining experiment with a monoclonal antibody against TfR (CD 71) and an antibody specific for red blood cells active in the synthesis of hemoglobin (GLY-A). Kuiper-Kramer et al [11]noted that this finding could be explained by increased cellularity and erythroid hyperplasia in the BM, reflecting an abundant amount of ineffective erythropoietic cells carrying decreased numbers of TfR on the cell membrane.…”

“…Kuiper-Kramer et al [11]noted that this finding could be explained by increased cellularity and erythroid hyperplasia in the BM, reflecting an abundant amount of ineffective erythropoietic cells carrying decreased numbers of TfR on the cell membrane. The findings of the present study support this possibility.…”

Enhancement of p53 gene transfer efficiency in hepatic tumor mediated by transferrin receptor through trans-arterial delivery

“…4,5 Transferrin receptor (TfR) is a transmembrane glycoprotein on the surface of cells and it serves as a ligand-receptor for transferrin (Tf ). [6][7][8] The human TfR is a homodimeric type II membrane protein consisting of two subunits covalently linked by intermolecular disulfide bonds. Each subunit has 760 amino acids, with a molecular weight of 90 kD.…”

“…In malignant cells however, there are elevated levels of TfR expression attributed to a requirement of high iron level for their growth, and also higher TfR affinity to Tf is indicated. [5][6][7][8] Therefore, a complex of Tf as a ligand in conjunction with the therapeutic gene, or even with other drugs and proteins, transported by the Tf-TfR system, may be target-delivered and transferred into the malignant cells. 5,10 However, for some solid tumors such as hepatic cancers, local drug delivery via adjacent arteries of interventional therapy may be a much more effective sitedirected delivery system than systemic injection.…”