Regulation of LMO2 mRNA and protein expression in erythroid differentiation

Abstract

new erythrocytes daily to replace the 1% of old cells removed from the circulation. Red cell production increases several-fold after blood loss or hemolysis but does not overshoot because it is so tightly regulated. This regulation involves three basic processes in erythroid progenitor and precursor cell populations: proliferation, differentiation, and survival. Although they act in concert from the earliest cell committed to erythropoiesis, the burst-forming unit-erythroid (BFU-E), through the last cell division of erythroblasts, each of these three processes can be regulated independently of another. After blood loss or hemolysis, stem cell factor (SCF/Kit-ligand) and glucocorticoids increase proliferation of cells in the BFU-E to colonyforming unit-erythroid (CFU-E) stages. 1 However, SCF and glucocorticoids have little effect on survival or differentiation of these erythroid progenitor cells. Erythopoietin (EPO), the major physiologic regulator of erythropoiesis, is regulated by hypoxia at the level of its transcription. 2 EPO promotes the survival of erythroid cells in the CFU-E through basophilic erythroblast stages without affecting their proliferation or differentiation. Contact with macrophages in erythroblastic islands regulates proliferation of these EPO-dependent cells without affecting their survival or differentiation. 3