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Blood, Vol. 92 No. 6 (September 15), 1998:
pp. 1859-1869
RAPID COMMUNICATION
Activation of p38 MAP Kinase and JNK But Not ERK Is Required for
Erythropoietin-Induced Erythroid Differentiation
Yuka Nagata,
Noriko Takahashi,
Roger J. Davis, and
Kazuo Todokoro
From the Tsukuba Life Science Center, The Institute of Physical and
Chemical Research (RIKEN), Ibaraki, Japan; and the Howard Hughes
Medical Institute, Program in Molecular Medicine, Department of
Biochemistry and Molecular Biology, University of Massachusetts Medical
School, Worcester, MA.
p38 MAP kinase (p38) and JNK have been described as playing a
critical role in the response to a variety of environmental stresses
and proinflammatory cytokines. It was recently reported that
hematopoietic cytokines activate not only classical MAP kinases (ERK),
but also p38 and JNK. However, the physiological function of these
kinases in hematopoiesis remains obscure. We found that all MAP kinases
examined, ERK1, ERK2, p38, JNK1, and JNK2, were rapidly and transiently
activated by erythropoietin (Epo) stimulation in SKT6 cells, which can
be induced to differentiate into hemoglobinized cells in response to
Epo. Furthermore, p38-specific inhibitor SB203580 but not MEK-specific
inhibitor PD98059 significantly suppressed Epo-induced differentiation
and antisense oligonucleotides of p38, JNK1, and JNK2, but neither ERK1
nor ERK2 clearly inhibited Epo-induced hemoglobinization. However, in
Epo-dependent FD-EPO cells, inhibition of either ERKs, p38, or JNKs
suppressed cell growth. Furthermore, forced expression of a
gain-of-function MKK6 mutant, which specifically activated p38, induced
hemoglobinization of SKT6 cells without Epo. These results indicate
that activation of p38 and JNKs but not of ERKs is required for
Epo-induced erythroid differentiation of SKT6 cells, whereas all of
these kinases are involved in Epo-induced mitogenesis of FD-EPO cells.
© 1998 by The American Society of Hematology.
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