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Activation of the stress-activated protein kinases by multiple
hematopoietic growth factors with the exception of interleukin-4
IN Foltz and JW Schrader
The Biomedical Research Centre, The University of British Columbia,
Vancouver, Canada.
The stress-activated protein/c-Jun N-terminal kinases (SAPK/JNK) have been
shown to be activated by pro-inflammatory cytokines, as well as physical
and chemical stresses. We now show that a variety of hematopoietic growth
factors, including Steel locus factor (SLF), granulocyte-macrophage
colony-stimulating factor (GM-CSF), and interleukin-3 (IL-3), all of which
promote the growth and survival of various lineages of hematopoietic cells,
activate the stress-activated protein kinases in the factor-dependent cell
line MC/9. These hematopoietic growth factors activated both 46- and 55-kD
isoforms of both SAPK gamma and SAPK alpha. Furthermore, we demonstrate
that SAPK activation correlated with the phosphorylation of SAPK/ERK
kinase-1 (SEK1) after treatment with SLF or GM-CSF. Interestingly, IL-4, a
cytokine with distinctive and important effects on the immune system, was
the exception among the hematopoietic growth factors we examined in failing
to induce activation of SAPK gamma, SAPK alpha, or SEK1. These findings
show that activation of SAPK is involved, not only in responses to
stresses, but also in signaling by growth factors that regulate the normal
development and function of cells of the immune system.
Volume 89,
Issue 9,
pp. 3092-3096,
05/01/1997
Copyright © 1997 by The American Society of Hematology
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