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EPO (aka. erythropoetin or hematopoietin ) is a glycoprotein hormone that controls erythropoiesis, or red blood cell production. It is a cytokine for erythrocyte (red blood cell) precursors in the bone marrow. It is produced by the peritubular capillary endothelial cells in the kidney, and is the hormone that regulates red blood cell production. It also plays an important role in the brain''s response to neuronal injury and wound healing.

A DNA sequence encoding the signal peptide and extracellular domain of human Erythropoietin receptor (EPO R, aa 1-250) was fused to the Fc region of human IgG1 (aa 93-330). The chimeric protein was expressed in modified human 293 cells.

Erythropoietin (EPO) regulates erythropoiesis, the differentiation of erythroid progenitor cells into mature red blood cells, and studies involving EPO deficient mice have confirmed that EPO is required for red blood cell development. Specifcally, EPO plays a role in erythroid progenitor cell survival, proliferation and differentiation, and induction of hemoglobin synthesis. EPO also stimulates proliferation of endothelial cells (i.e. it has a pro-angiogenic effect) and B- cells, stimulates megakaryocytopoiesis, and has neurotrophic, neuroprotective and cardioprotective properties. The effects of EPO are exerted through binding to the EPO receptor (EPO R). EPO R is a 508 amino acid type I transmembrane receptor with a molecular weight of 55kDa and contains a potential N-linked glycosylation site. It is predominantly expressed on pluripotent embryonic stem cells and early multipotent hematopoietic cells as well as in other tissues such as brain, spinal cord, kidney, lung and pancreas. The expression of EPO R is downregulated in a number of disease states such as endometriosis, in which relatively low levels of EPO R are detected in the peritoneal lesions of patients with stage I of the disease, and autosomal dominant erythrocytosis, in which a truncated EPO R increases EPO sensitivity and elevates the production of red blood cells. However EPO R expression has also been observed in many human cancers including uterine, ovarian, mammary, colon, lung, and prostate cancers, melanoma, and hematological malignancies such as leukemias. Furthermore, the administration of EPO-EPO R antagonists can inhibit the growth of cancer cells in vivo, suggesting that EPO signalling may facilitate the progression of human malignant disease states. For a recent review please refer to Bartesaghi S, Marinovich M, Corsini, E, Galli CL, Viviani B. (2004) Neurotoxicity 26(5):923-8.