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Blood, Vol. 93 No. 2 (January 15), 1999:
pp. 537-553
Synergistic Activation of Mitogen-Activated Protein Kinase by Cyclic
AMP and Myeloid Growth Factors Opposes Cyclic AMP's Growth-Inhibitory
Effects
Angel Wai-mun Lee
From the Department of Biochemistry and Molecular Biophysics,
Washington University Medical School, St Louis, MO.
Colony-stimulating factors (CSFs) promote the proliferation,
differentiation, commitment, and survival of myeloid progenitors, whereas cyclic AMP (cAMP)-mediated signals frequently induce their growth arrest and apoptosis. The ERK/mitogen-activated protein kinase
(MAPK) pathway is a target for both CSFs and cAMP. We investigated how
costimulation by cAMP and colony-stimulating factor-1 (CSF-1) or
interleukin-3 (IL-3) modulates MAPK in the myeloid progenitor cell
line, 32D. cAMP dramatically increased ERK activity in the presence of
CSF-1 or IL-3. IL-3 also synergized with cAMP to activate ERK in
another myeloid cell line, FDC-P1. The increase in ERK activity was
transmitted to a downstream target, p90rsk. cAMP treatment
of 32D cells transfected with oncogenic Ras was found to recapitulate
the superactivation of ERK seen with cAMP and CSF-1 or IL-3. ERK
activation in the presence of cAMP did not appear to involve any of the
Raf isoforms and was blocked by expression of dominant-negative MEK1 or
treatment with a MEK inhibitor, PD98059. Although cAMP had an overall
inhibitory effect on CSF-1-mediated proliferation and survival, the
inhibition was markedly increased if ERK activation was blocked by
PD98059. These findings suggest that upregulation of the ERK pathway is
one mechanism induced by CSF-1 and IL-3 to protect myeloid progenitors
from the growth-suppressive and apoptosis-inducing effects of cAMP elevations.
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