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Developmental regulation of erythropoiesis by hematopoietic growth factors:
analysis on populations of BFU-E from bone marrow, peripheral blood, and
fetal liver
SG Emerson, S Thomas, JL Ferrara and JL Greenstein
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
Fetal hematopoiesis is characterized by expanding erythropoiesis to support
a continuously increasing RBC mass. To explore the basis for this anabolic,
nonhomeostatic erythropoiesis, the proliferative effect of recombinant
hematopoietic growth factors on highly enriched hematopoietic progenitor
cells from fetal and adult tissues were compared. Fetal hepatic BFU-E,
unlike adult bone marrow (BM) or peripheral blood (PB) BFU-E, were capable
of proliferating in response to erythropoietin in the absence of added GM
colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3), and
erythropoietin (Epo) directly stimulated the expansion of the fetal BFU-E
pool in suspension culture. A murine monoclonal antibody (MoAb), Ep 3, was
raised against enriched fetal liver progenitor cells, which detected all
fetal BFU-E and which reacted with the erythropoietin-responsive,
GM-CSF/IL-3-independent fraction of adult BM BFU-E and CFU-E. All adult PB
BFU-E were Ep 3- but became Ep 3+ after stimulation with GM-CSF or IL-3.
These data indicate that Epo plays a unique role in fetal hepatic
erythropoiesis, stimulating proliferation of immature BFU-E in addition to
promoting terminal differentiation of later erythroid progenitor cells. In
addition, these results demonstrate a MoAb which detects all
erythropoietin-responsive progenitor cells and distinguishes the BFU-E
compartments in adult BM and PB.
Volume 74,
Issue 1,
pp. 49-55,
07/01/1989
Copyright © 1989 by The American Society of Hematology
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