Glucocorticoids inhibit the growth of murine fetal liver erythroid burst-forming cells.

Abstract

The effects of glucocorticoids on the formation of large colonies of erythroid cells, termed "bursts," by erythroid burst-forming units (BFU-E) obtained from murine fetal liver were studied in plasma clot cultures. Fetal liver erythroid progenitor cells formed a reduced number of erythroid bursts when cultured for 9 days in the presence of dexamethasone. Similar results were obtained with other glucocorticoids, including corticosterone, cortisol, prednisone, prednisolone, and 9 alpha-fluorocortisol; in contrast, neither 11 alpha-cortisol, tetrahydrocortisol, nor progesterone influenced erythroid burst formation. Erythroid burst formation was also decreased by the addition of dexamethasone on days 5, 7, and 9 to developing erythroid bursts, indicating that the growth of BFU-E-derived erythroid precursor cells was also reduced by the glucocorticoid. The formation of erythroid bursts by murine fetal liver cells was also reduced when the cells were incubated with dexamethasone (10(-7) and 10(-8) M) for 1 h, washed, and cultured in plasma clots; the concentration of dexamethasone was reduced by the washes to levels which do not inhibit the growth of BFU-E derived erythroid progenitor cells. Similar results were obtained with various other glucocorticoids (10(-7) M). These studies demonstrate that glucocorticoids exert a suppressive effect on the formation of erythroid bursts by murine fetal liver erythroid progenitor cells, and that this effect is the net result of inhibitory effects on the BFU-E and its progeny.