Transcriptional activation of the γ-globin gene in baboons treated with decitabine and in cultured erythroid progenitor cells involves different mechanisms

The mechanism responsible for increased γ-globin expression in cultured EPC was unexpectedly not associated with increased DNA hypomethylation of the γ-globin gene promoter compared to normal BM erythroid cells, in contrast to BM erythroid cells of decitabine-treated baboons. Rather, increased fetal hemoglobin in EPC cultures was associated with a fetal Iγ/Vγ chain ratio and a difference in the size of the BCL11A protein compared to normal BM erythroid cells.