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Heparin inhibits the expression of interleukin-11 and granulocyte-
macrophage colony-stimulating factor in primate bone marrow stromal
fibroblasts through mRNA destabilization
L Yang and YC Yang
Department of Biochemistry, Walther Oncology Center, Indiana University
School of Medicine, Indianapolis 46202, USA.
Interactions between different cytokines, extracellular matrix components,
and various cell types inside the bone marrow microenvironment are believed
to play important roles in the regulation of hematopoiesis. We observed
that both interleukin-1 (IL-1) and 12-O- tetradecanoylphorbol-13-acetate
(TPA) can stimulate the expression of IL-11 and granulocyte-macrophage
colony-stimulating factor (GM-CSF) genes in a primate bone marrow stromal
fibroblast cell line, PU-34. We also found that IL-1 or TPA-stimulated
IL-11 and GM-CSF expression in PU-34 cells can be abolished by heparin, a
class of molecules related to extracellular matrix components,
glycosaminoglycans. Because the growth inhibitory signals provided by
extracellular factors were less understood, the mechanisms of heparin
inhibition of IL-11 and GM-CSF gene expression were further investigated.
Our data demonstrate for the first time that heparin did not alter the
transcription of endogenous IL-11 and GM-CSF genes or an exogenous IL-11
promoter construct containing an AP-1 sequence. Instead, heparin
facilitated the degradation of the corresponding mRNAs. Through RNA gel
shift assays, heparin-mediated mRNA destabilization was tentatively linked
to its competition for mRNA binding proteins both in the cell-free system
and in intact cells. Collectively, our findings suggest that varying
degrees of heparin inhibition may provide a novel mechanism for the
regulation of cytokine expression during the growth and differentiation of
different lineages of hematopoietic cells.
Volume 86,
Issue 7,
pp. 2526-2533,
10/01/1995
Copyright © 1995 by The American Society of Hematology
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