Effect of dexamethasone on fetal liver erythroid colony-forming cells in vivo.

Pretreatment of pregnant mice (CD-1) with intravenous dexamethasone phosphate (10(-3)-10(-7) g/mouse), a synthetic glucocorticoid, reduced the number of erythroid colonies that formed when 15-day-old fetal liver erythroid progenitor cells (3 X 10(4] were cultured for two days in plasma clots containing exogenous erythropoietin (Epo) (25 mU). The proliferative rate of fetal liver erythroid colony-forming cells (CFU-E), obtained from pregnant mice treated 24 h earlier with dexamethasone phosphate (1 mg/mouse), was reduced from 76% (control) to 46% as measured by a decrease in the percentage of fetal liver CFU-E lost following a 20-min exposure to high-specific-activity tritiated thymidine (50 microCi, 50-77 Ci/mmol). In addition, pretreatment of pregnant mice with lower doses of dexamethasone phosphate (10(-5)-10(-7) g/mouse) resulted in a higher percentage of fetal liver CFU-E lost following exposure to high-specific-activity tritiated thymidine (64% and 67%, respectively). Concomitantly, the inhibitory effect of dexamethasone on erythroid colony formation by these fetal liver cells in response to exogenous Epo is reduced. These results appear to indicate that the dexamethasone-mediated reduction in erythroid colony formation is inversely related to the fraction of fetal liver CFU-E lost after exposure to high-specific-activity tritiated thymidine. Furthermore, this observation suggests that glucocorticoids inhibit erythroid colony formation by decreasing the proliferative rate of the fetal liver CFU-E.