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Blood, Vol. 94 No. 3 (August 1), 1999:
pp. 853-863
Requirement of Activation of JNK and p38 for Environmental
Stress-Induced Erythroid Differentiation and Apoptosis and of
Inhibition of ERK for Apoptosis
Yuka Nagata and
Kazuo Todokoro
From the Tsukuba Life Science Center, The Institute of Physical and
Chemical Research (RIKEN), Tsukuba, Ibaraki, Japan.
C-Jun amino terminal kinase/stress-activated protein kinases
(JNK/SAPK) and p38 subgroups of mitogen-activated protein kinases have
been suggested to play a critical role in apoptosis, cell growth,
and/or differentiation. We found that a short exposure of SKT6 cells,
which respond to erythropoietin (Epo) and induce erythroid
differentiation, to osmotic or heat shock induced transient activation
of JNK/SAPK and p38 and inactivation of ERK and resulted in erythroid
differentiation without Epo, whereas long exposure of the cells to
these stresses induced prolonged activation/inactivation of the same
kinases and caused apoptosis. Inhibition of JNK/SAPK and p38 resulted
in inhibition of stress-induced erythroid differentiation and
apoptosis. Inhibition of ERK had no effect on stress-induced erythroid
differentiation, but stimulated apoptosis. Activation of p38 and/or
JNK/SAPK for a short time caused erythroid differentiation without Epo,
although its prolonged activation induced apoptosis. Activation of ERK
suppressed stress-induced apoptosis. These results indicate that short
cellular stresses, inducing transient activation of JNK/SAPK and p38,
lead to cell differentiation rather than apoptosis. Furthermore,
activation of JNK/SAPK and p38 is required for both cell
differentiation and apoptosis, and the duration of their activation may
determine the cell fate, cell differentiation, and apoptosis. In
contrast, inactivation of ERK is required for stress-induced apoptosis
but not cell differentiation.
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