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Transforming growth factor beta (TGF-beta), a potent inhibitor of
erythropoiesis: neutralizing TGF-beta antibodies show erythropoietin as a
potent stimulator of murine burst-forming unit erythroid colony formation
in the absence of a burst-promoting activity
I Dybedal and SE Jacobsen
Institute of Cancer Research, University of Trondheim, Norway.
Transforming growth factor beta (TGF-beta) is a bifunctional regulator of
the growth of myeloid progenitors and is here demonstrated to directly
inhibit the growth of primitive erythroid progenitors by 95% to 100%
regardless of the cytokines stimulating growth. Autocrine TGF- beta
production of primitive hematopoietic progenitors has previously been
reported. In the present study, a neutralizing TGF-beta antibody
(anti-TGF-beta) added to serum-containing cultures, resulted in a 3-, 4- ,
and 25-fold increase in burst-forming unit erythroid (BFU-E) colony
formation in response to interleukin-4 (IL-4) plus erythropoietin (Epo),
SCF plus Epo, and IL-11 plus Epo, respectively. The growth of BFU-E
progenitors has been suggested to require a burst-promoting activity in
addition to Epo. Accordingly, we observed no BFU-E colony formation in
serum-containing cultures in response to Epo alone. In contrast, 50 BFU-E
colonies were formed when anti-TGF-beta was included in the culture. In
serum-free cultures, Epo also stimulated BFU-E colony formation in the
absence of other cytokines, whereas anti-TGF- beta had no effect on the
number of colonies formed. Quantitation of TGF-beta 1 in serum by an
enzyme-linked immunosorbent assay method showed predominantly the presence
of precursor (latent) TGF-beta 1, but also showed active TGF-beta 1 at a
concentration sufficient to potently inhibit erythroid colony formation.
Thus, neutralization of active TGF- beta 1 in serum shows that Epo alone is
sufficient to stimulate the growth of murine BFU-E progenitors.
Volume 86,
Issue 3,
pp. 949-957,
08/01/1995
Copyright © 1995 by The American Society of Hematology
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