Erythroid differentiation of adult hematopoietic progenitor cells requires stimulation by erythropoietin, a hypoxia inducible cytokine that promotes erythroid progenitor cell survival, proliferation, differentiation and hemoglobin production. Erythropoietin binds to its cell surface receptor and induces transcription factors that regulate erythroid gene expression such as the general erythroid factor GATA-1, the basic helix-loop-helix transcription factor, Tal1, and EKLF which is relatively specific for beta-globin expression. As with increased Epo stimulation, increased expression of erythropoietin receptor promotes erythropoiesis and globin gene transcription. A potential interplay between erythropoiesis and glucose metabolism is suggested by erythropoietin treatment in mice that reduces blood glucose in addition to increasing hematocrit. We observed that increased Epo directly affected glucose uptake in differentiating erythroid progenitor while glucose supplementation in erythropoietin stimulated erythroid progenitor cell cultures affected cell proliferation. These data suggest that in addition to Epo reduction in blood glucose, elevated glucose level may affect the erythropoietin erythropoietic response.

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