AJP - Cell Physiology, Vol 267, Issue 1 C25-C31, Copyright © 1994 by American Physiological Society
TGF-beta-induced macrophage colony-stimulating factor gene expression in various mesenchymal cell lines
T. Takaishi, T. Matsui, T. Tsukamoto, M. Ito, T. Taniguchi, M. Fukase and K. Chihara
Department of Medicine, Kobe University School of Medicine, Japan.
We report here that transforming growth factor-beta (TGF-beta) can increase
the expression level of macrophage colony-stimulating factor (M-CSF) mRNA
in a variety of mesenchymal cell lines derived from osteoblasts, bone
marrow stromal cells, fibroblasts, and myoblasts. The M-CSF activity in the
conditioned medium of mouse osteoblast-like MC3T3-E1 cells was increased by
TGF-beta as well as interleukin-1 (IL-1) treatment. The increase of M-CSF
mRNA expression was observed as early as 2 h after TGF-beta or IL-1
addition and was superinduced by cycloheximide treatment. Nuclear run-off
assays revealed that the increase in M-CSF mRNA by TGF-beta as well as IL-1
occurred, at least in part, at the transcriptional level. Platelet-derived
growth factor (PDGF) also enhanced the M-CSF production in MC3T3-E1 cells.
Furthermore, TGF-beta and IL-1 distinctly induced both PDGF-A and PDGF-B
chain mRNA in MC3T3-E1 with different time courses. Our present studies
suggest that PDGF autocrine loop-dependent and loop-independent pathways
could modulate the M-CSF production stimulated by TGF-beta or IL-1 and
account for the complexity of the cytokine network involving M-CSF in vivo
under various physiological and pathological conditions.
