Insulin and insulin‐like growth factor I support the proliferation of erythroid progenitor cells in bone marrow through the sharing of receptors

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Abstract
The effects of insulin and insulin‐like growth factor I (IGF‐I) on the proliferation of erythroid progenitor cells in bone marrow were studied in serum‐deprived culture. Primitive human bone marrow cells were purified by cell sorting on the basis of the expression of CD34 and the Kit receptor. Insulin and IGF‐I with erythropoietin (EPO) dose dependently supported the formation of erythroid colonies of CD34+/Kit+ cells in bone marrow. The direct effect of insulin and IGF‐I on the stimulation of primitive erythroid progenitor cells was confirmed by single‐cell proliferation studies in serum‐deprived liquid suspension culture. The addition of insulin and/or IGF‐I to stem cell factor (SCF) resulted in an additive increase in the number of erythroid colonies. The erythroid colonies formed by insulin and IGF‐I with EPO were different in size from those formed by SCF with EPO. These findings imply that erythroid progenitor cells responding to insulin and IGF‐I might be at a different developmental stage of erythropoiesis from those responding to SCF in CD34+/Kit+ cells. Similarly, insulin and IGF‐I with EPO supported the proliferation of the mature erythroid progenitor cells in light‐density bone marrow mononuclear cells (LDBMCs). The addition of the anti‐receptor antibody to IGF‐I receptor or insulin receptor partially suppressed erythroid colony formation supported with insulin or IGF‐I in both CD34+/Kit+ cells and LDBMCs. The simultaneous addition of both receptor antibodies completely abrogated the erythroid colony formation. These results suggest that insulin and IGF‐I directly stimulate the proliferation of the late stage of primitive erythroid progenitor cells and mature erythroid progenitor cells through the sharing of receptors.