Activation of the vitamin D receptor transcription factor stimulates the growth of definitive erythroid progenitors

Blood Advances
Jeffrey BarminkoMargaret H Baron

Abstract

The pathways that regulate the growth of erythroid progenitors are incompletely understood. In a computational analysis of gene expression changes during erythroid ontogeny, the vitamin D receptor (Vdr) nuclear hormone receptor transcription factor gene was identified in fetal and adult stages, but not at the embryonic stage of development. Vdr was expressed in definitive erythroid (EryD) progenitors and was downregulated during their maturation. Activation of Vdr signaling by the vitamin D3 agonist calcitriol increased the outgrowth of EryD colonies from fetal liver and adult bone marrow, maintained progenitor potential, and delayed erythroid maturation, as revealed by clonogenic assays, suspension culture, cell surface phenotype, and gene expression analyses. The early (cKit+CD71lo/neg), but not the late (cKit+CD71hi), EryD progenitor subset of LinnegcKit+ cells was responsive to calcitriol. Culture of cKit+CD71lo/neg progenitors in the presence of both vitamin D3 and glucocorticoid receptor ligands resulted in an increase in proliferation that was at least additive compared with either ligand alone. Lentivirus shRNA-mediated knockdown of Vdr expression abrogated the stimulation of early erythroid progenitor growth by calcitr...Continue Reading

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