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Basic fibroblast growth factor promotes the proliferation of human
megakaryocyte progenitor cells
E Bruno, RJ Cooper, EL Wilson, JL Gabrilove and R Hoffman
Department of Medicine of the Indiana University School of Medicine,
Indianapolis.
Basic fibroblast growth factor (bFGF), a multifunctional growth factor
produced by bone marrow stromal cells, is known to be a potent modulator of
hematopoiesis. Because bFGF is present in both human megakaryocytes (MKs)
and platelets, we have hypothesized that this growth factor might affect
human megakaryocytopoiesis. To test this hypothesis, either low density
bone marrow (BM) cells (LDBM), a human BM subpopulation (CD34+ DR+)
enriched for the colony-forming unit megakaryocyte (CFU-MK) or a BM
subpopulation (CD34+ DR-) enriched for the more primitive burst-forming
unit megakaryocyte (BFU-MK) were assayed in the presence of this growth
factor. The effect of bFGF on MK colony formation differed according to the
cell population assayed. bFGF alone had on MK colony-stimulating activity
(MK-CSA) when either CD34+ DR+ or CD34+ DR- BM cells were cloned, but
exhibited MK-CSA equivalent to that of interleukin-3 (IL-3) when LDBM cells
were used as the target cell population. The MK-CSA of bFGF was inhibited
by the addition of neutralizing antisera to either IL-3 and/or granulocyte-
macrophage colony-stimulating factor (GM-CSF) but not IL-6. The addition of
excess amounts of either IL-3 or GM-CSF to cultures containing bFGF plus
anti-IL-3 or anti-GM-CSF reversed the inhibition by the corresponding
antisera. The addition of bFGF and IL-3 to assays containing CD34+ DR+ or
CD34+ DR- cells increased the size of both CFU- MK- and BFU-MK-derived
colonies, respectively, when compared with assays containing IL-3 alone.
This increase in MK colony size mediated by bFGF was not affected by
addition of either an anti-GM-CSF or anti- IL-6 neutralizing antisera. When
LDBM cells were assayed, bFGF alone increased CFU-MK-derived colony size
when compared with control values. However, this potentiation of MK colony
size by bFGF could be reversed by the addition of either anti-IL-3 or
anti-GM-CSF but not anti-IL-6 antisera. In addition, the effects of bFGF
and IL-3 on the size of MK colonies cloned from LDBM were not additive.
These results suggest that bFGF affects human megakaryocytopoiesis by
directly promoting MK progenitor cell proliferation and stimulating BM
accessory cells to release growth factor(s) with MK-CSA, such as IL-3 and
GM-CSF. We conclude that bFGF, likely produced by cellular components of
the BM microenvironment, plays an important role in the control of human
megakaryocytopoiesis.
Volume 82,
Issue 2,
pp. 430-435,
07/15/1993
Copyright © 1993 by The American Society of Hematology
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