Abstract
Erythropoiesis is regulated by erythropoietin (Ep), a glycoprotein hormone produced in the kidneys and to a lesser extent in the liver, which promotes the proliferation and differentiation of committed erythroid progenitor cells. Ep is not the only growth factor which interacts with erythroid progenitor cells, but it is the most important, and a lack of it is associated clinically with severe anemia, while in vitro, erythroid progenitor cells cannot survive without it. Ep is unique amongst hematopoietic growth factors for several reasons. It was the first one to be identified (Reissmann 1956) and the only one which fits the definition of a hormone. In contrast to the other hematopoietic growth factors, Ep was not initially recognized as a colony stimulating factor and has no influence on the behavior of the mature progeny of its target cells. With perhaps the exception of macrophage colony stimulating factor (CSF-1), Ep is more restricted in its progenitor cell nteractions than any other hematopoietic growth factor. Interestingly, Ep also shares in common with CSF-1 and granulocyte colony stimulating factor (G-CSF) the expression of its receptors by cells of placental origin (Muller et al. 1983; Rettenmier et al. 1986; Koury et al. 1988; Uzumaki et al. 1989). Although the reason for placental expression is unknown, it is noteworthy that the CSF-1 receptor is the product of the c-fms protooncogene (Sherr et al. 1985).
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Spivak, J.L. (1992). The Mechanism of Action of Erythropoietin: Erythroid Cell Response. In: Fisher, J.W. (eds) Biochemical Pharmacology of Blood and Bloodforming Organs. Handbook of Experimental Pharmacology, vol 101. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75865-2_4
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