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This article was retracted on June 15, 2006.
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Macrophage inflammatory protein-1alpha and interferon-inducible protein 10
inhibit synergistically induced growth factor stimulation of MAP kinase
activity and suppress phosphorylation of eukaryotic initiation factor 4E
and 4E binding protein 1
SM Aronica, AC Gingras, N Sonenberg, S Cooper, N Hague and HE Broxmeyer
Department of Microbiology/Immunology, Walther Oncology Center, Indiana
University School of Medicine, Indianapolis 46202-5121, USA.
Granulocyte-macrophage colony-stimulating factor (GM-CSF) and Steel factor
(SLF) synergistically stimulate Raf-1 kinase activity, protein synthesis,
and proliferation in hematopoietic MO7e cells; synergistic action of these
factors is blocked by the suppressive chemokines macrophage inflammatory
protein-1alpha (MIP-1alpha) and interferon- inducible protein 10 (IP-10;
Aronica et al, J Biol Chem 270:21998, 1995). We assessed the potential for
both stimulatory and inhibitory factors to act through the MAP kinase
signaling pathway by studying the effects of growth factors and chemokines
on MAP kinase activation. Also, because activation of kinase signaling
pathways and stimulation of protein synthesis by peptide growth factors are
associated with increased phosphorylation of eukaryotic initiation factor
4E (elF-4E) and the translational repressor 4E-binding protein 1 (4E-BP1)
in some target cells, we investigated whether growth factor treatment could
alter eIF-4E or 4E-BP1 phosphorylation state in MO7e cells. We report that
treatment of MO7e cells with GM-CSF and SLF stimulated significant,
greater-than-additive increases in MAP kinase activity and the
phosphorylation of both eIF-4E and 4E-BP1. Increased 4E-BP1 phosphorylation
correlated with a decrease in the association of 4E-BP1 with eIF-4E. Growth
factor-induced phosphorylation of 4E-BP1 and dissociation of 4E-BP1 from
eIF-4E was blocked in cells treated with rapamycin, wortmannin, or
PD098059. Treatment of cells with IP-10 or MIP-1alpha blocked the
stimulatory effects of GM-CSF and SLF, resulting in suppression of MAP
kinase activity, eIF-4E and 4E-BP1 phosphorylation, and eIF-4E/4E-BP1
dissociation. Our results suggest that GM-CSF and SLF exert part of their
combined growth-promoting effects on MO7e cells through activation of MAP
kinase and enhancement of eIF-4E and 4E-BP1 phosphorylation and
dissociation and that suppression of growth factor-induced protein
synthesis by MIP-1alpha and IP-10 involves translational repression at the
level of eIF-4E.
Volume 89,
Issue 10,
pp. 3582-3595,
05/15/1997
Copyright © 1997 by The American Society of Hematology
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