Hb F Production in Stressed Erythropoiesis: Observations and Kinetic Modelsaa

摘要: The mechanism of stimulation Hb F in stressed erythropoiesis is examined. Conditions known to produce a transient elevation F-cells (acute anemia; acute expansion; treatment with cytotoxic compounds) have common element, the kinetic perturbations erythroid differentiation/maturation they trigger. Cell cycling must be shortened and total time differentiation (from BFUe erythroblast) shortened. We propose that are formed either because shortening or cell cycle cells. With model F-cell formation attributed "premature commitment" progenitors. gamma-gene expression occurs chromatin changes normally inactivate gamma genes not completed critical divisions which inactivated skipped. faster explains by assuming transcription activated when (and especially duration G0/G1) progenitors erythroblasts falls below time. proposed models can readily explain normal adult as products random deviation from kinetics. two also chronic erythropoietic stress (chronic hemolytic anemias, patients hemoglobinopathies). Differences degree such may reflect differences intensity perturbation their erythropoiesis.