Erythroid precursor cells

BiUco N. (1997) Culture of erythroid precursor cells of individuals exposed to ionizing radiation. Cytology and Genetics. Allerton Press, inc.New York 31, 5, 54-59. 

Erythropoietin is a protein produced mainly in the cortex of the kidney. Erythropoietin binds to a receptor on the surface of erythroid precursor cells. It stimulates erythropoiesis and is primarily indicated for the treatment of anemia in patients with chronic renal failure. Other indications are the management of anemia in cancer patients and in HIV positive subjects treated with anti-HIV regimens. 

It exerts its action by binding to receptor on surface of erythroid precursor cells. There is increase in intracellular concentration of calcium and arachidonate and changes in intracellular phosphorylation. It stimulates proliferation, maturation and haemoglobin formation by committed erythroid progenitors. 

Fig. 4. In situ hybridization technique. Part of an erythroid precursor cell infected with the human parvovirus B19 and probed for viral DNA. The BI9 nucleic acid is located within the centra electron lucent area of the nucleus (N) and also at nuclear pores (arrowheads). Ch, chromatin M, mitochondrion. A three-step detection protocol was used (see ref. 5 for details). Sheep antidigoxigenin followed by rabbit antisheep Ig and then goat antirabbit Ig conjugated to 10-nm gold. Bar is 0.5 pm.

The v-erbB oncogene acts to expand a pool of highly mitotic, undifferentiated erythroid precursor cells, but these are poorly tumorigenic, because they differentiate at high rates into postmitotic, end-stage red cells. Another potential oncogene, v-erbA, blocks differentiation of erythroid precursors but creates no tumors because it is unable to provide the mitogenic impetus needed to expand the pool of stem... 

D. Metcalf, G. R. Johnson, and A. W. Burgess, Direct stimulation by purified GM-CSF of the proliferation of multipotential and erythroid precursor cells. Blood 55 (1980), 138-147. 

Human erythropoietin (hEpo) is a glycoprotein of 36,000 daltons, produced by the kidney in response to hypoxia. It regulates the rate of production of mature erythrocytes by stimulating the proliferation and differentiation of erythroid precursor cells. Renal failure leads to lack of this growth factor which, in turn, leads to anemia (Hillman, 1990 Cotes and Spivak, 1991). 

In 11 hemodialysis patients who also received recombinant human erythropoietin for anemia secondary to renal failure, deferoxamine increased the proliferation of erythroid precursor cells and had a synergistic in vivo effect on eiythropoietin (79,80). 

The hormone EPO, 90% of which is produced by the kidneys, initiates and stimulates the production of RBCs. Erythropoiesis is driven by a feedback loop. The main mechanism of action of EPO is to prevent apoptosis, or programmed cell death, of erythroid precursor cells and to allow their proliferation and subsequent maturation. A decrease in tissue oxygen concentration signals the kidneys to increase the production and release of EPO into the plasma, which (1) stimulates stem cells to differentiate into proerythroblasts, (2) increases the rate of mitosis, (3) increases the release of reticulocytes from the marrow, and (4) induces Hgb formation. In normal circumstances, the RBC mass is kept at an almost constant level by EPO matching new erythrocyte production to the namral rate of loss of RBCs. Accelerated Hgb synthesis makes it possible to achieve the critical Hgb concentration necessary for RBCs to mature more rapidly, and a feedback mechanism stops further RBC nucleic acid synthesis, causing an earlier release of reticulocytes. Early appearance of large quantities of reticulocytes in the peripheral circulation (reticulocytosis) is another indication of increased RBC production. 

Mufson R A, Gesner T G (1987). Binding and internalization of recombinant hnman erythropoietin in murine erythroid precursor cells. Blood. 69 1485-1490. 

Enhances the proliferation of T lymphocytes, mass cells, erythroid precursor cells, and megakaryoblastic leukemia cells... 

No laboratory tools are presently available to identify the drug responsible for triggering aplastic anemia in an individual case. Accordingly, the diagnosis is based on the finding of pancytopenia in the peripheral blood and deficiency of myeloid and erythroid precursor cells in the bone marrow. 

Zhou, X, Morreau, H., d Azzo, A. et al (1995) Mouse model for the lysosomal disorder galactosiaUdosis and correction of the phenotype with overexpressing erythroid precursor cells. Genes and Development, 9,2623-2634. 

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