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Transforming growth factor-beta 1 bifunctionally regulates murine
macrophage proliferation
K Fan, Q Ruan, L Sensenbrenner and B Chen
Department of Internal Medicine, Wayne State University School of Medicine,
Detroit, MI 48202.
Transforming growth factor-beta (TGF-beta) is a family of polypeptide
growth factors with multiple functional activities. Recent studies suggest
that TGF-beta is a selective inhibitor of hematopoietic cells. In this
report, we study the effect of TGF-beta 1 on the proliferation of murine
peritoneal exudate macrophages (PEM) in response to purified murine
recombinant granulocyte-macrophage colony-stimulating factor (rMuGM-CSF)
and human recombinant M-CSF (rHuM-CSF). In mice, PEM and other types of
tissue macrophages display multiple types of receptors for CSFs and respond
to them, either alone or in combination, to undergo extensive proliferation
in vitro. Recombinant human TGF-beta 1 (rHuTGF-beta 1) (0.1 to 1.0 ng/mL)
markedly enhanced the growth of PEM in response to rMuGM-CSF but inhibited
their responsiveness to rHuM- CSF. Similar effects of rHuTGF-beta 1 were
also detected using murine pulmonary alveolar macrophages (PAM) and bone
marrow-derived macrophages (BMDM). Receptor binding assays using iodinated
rMuGM-CSF and rHuM-CSF showed that rHuTGF-beta 1 treatment greatly enhanced
the expression of GM-CSF receptors in PEM, in a time- and dose-dependent
manner, suggesting a possible mechanism for the synergistic effect of
TGF-beta 1. On the other hand, the expression of M-CSF receptors was not
affected by TGF-beta 1 treatment. Analysis by mRNA PCR showed that the
synergistic effect of TGF-beta 1 is not due to autocrine CSFs produced by
treated cells. Our results suggest that TGF-beta 1 is an important
regulator of macrophage proliferation. Depending on the types of CSFs
present, TGF-beta 1 may act either as a growth promoter or inhibitor.
Volume 79,
Issue 7,
pp. 1679-1685,
04/01/1992
Copyright © 1992 by The American Society of Hematology
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