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Blood, Vol. 96 No. 3 (August 1), 2000:
pp. 933-940
JNK and p38 are activated by erythropoietin (EPO) but are not
induced in apoptosis following EPO withdrawal in EPO-dependent
HCD57 cells
Sarah M. Jacobs-Helber,
John J. Ryan, and
Stephen
T. Sawyer
From the Department of Pharmacology/Toxicology, Medical College of
Virginia Campus, Richmond, VA; and the Department of Biology, Virginia
Commonwealth University, Richmond, VA.
Jun N-terminal kinase (JNK) and p38, members of the
mitogen-activated protein kinase family of serine/threonine
kinases, are activated as a result of cellular stress but may
also play a role in growth factor-induced proliferation and/or survival
or differentiation of many cells. A recent report has
implicated JNK and p38 in the induction of apoptosis in the
erythropoietin (EPO)-dependent erythroid cell line HCD57 following EPO
withdrawal, whereas our previously reported data did not support
a role for JNK in growth factor withdrawal-induced apoptosis in HCD57
cells. Therefore, further testing was done to see if JNK was
activated in EPO withdrawal-induced apoptosis; the study was extended
to p38 and characterized the effect of EPO on JNK and p38
activities. Treatment of HCD57 cells with EPO resulted in a
gradual and sustained activation of both JNK and p38 activity; these
activities decreased on EPO withdrawal. Transient activation of p42/p44
extracellular signal-related kinases (ERK) was also detected.
Inhibition of ERK activity inhibited proliferation in EPO-treated cells
but neither induced apoptosis nor activated JNK. Inhibition of p38
activity inhibited proliferation but did not protect HCD57 cells from
apoptosis induced by EPO withdrawal. Treatment of HCD57 cells with
tumor necrosis factor-alpha induced JNK activation but did not induce
apoptosis. These results implicate JNK, p38, and ERK in EPO-induced
proliferation and/or survival of erythroid cells but do not support a
role for JNK or p38 in apoptosis induced by EPO withdrawal from
erythroid cells.
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