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Activation of JNK signaling pathway by erythropoietin, thrombopoietin, and
interleukin-3
Y Nagata, E Nishida and K Todokoro
Tsukuba Life Science Center, The Institute of Physical and Chemical
Research (RIKEN), Ibaraki, Japan.
A variety of environmental stresses, such as osmotic shock, UV radiation,
and heat shock, or the proinflammatory cytokines tumor necrosis
factor-alpha and interleukin-1 reportedly induce activation of c-Jun
amino-terminal kinases (JNK), which are usually activated by SEK1/MKK4. We
report here that the hematopoietic cytokines interleukin- 3 (IL-3),
erythropoietin (Epo), and thrombopoietin (Tpo), which regulate growth and
differentiation of hematopoietic progenitor cells, erythroids, and
megakaryocytes/platelets, respectively, also activate a JNK signaling
cascade. In-gel kinase assay as well as in vitro kinase assay clearly
showed that IL-3, Epo, and Tpo rapidly and transiently activated both JNK1
and JNK2 in IL-3-, Epo-, or Tpo-dependent mouse hematopoietic progenitor
cells. However, immunoblot analysis and in vitro kinase assay showed that
neither phosphorylation nor activation of SEK1/MKK4 was induced by IL-3,
Epo, or Tpo stimulation. Therefore, we concluded that the JNK signaling
cascade plays an important role not only in stress responses and
proinflammatory cytokine actions but also in hematopoietic cytokine actions
and that hematopoietic cytokines may activate the JNKs through a kinase
other than SEK1/MKK4, as previously suggested for stress-activated cells.
Volume 89,
Issue 8,
pp. 2664-2669,
04/15/1997
Copyright © 1997 by The American Society of Hematology
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