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J Biol Chem, Vol. 275, Issue 15, 11418-11424, April 14, 2000
From the Pulse treatment of U-937 promonocytic cells with
cadmium chloride (2 h at 200 µM) provoked apoptosis
and induced a rapid phosphorylation of p38 mitogen-activated protein
kinase (p38MAPK) as well as a late phosphorylation of
extracellular signal-regulated protein kinases (ERK1/2). However,
although the p38MAPK-specific inhibitor SB203580 attenuated
apoptosis, the process was not affected by the ERK-specific inhibitor
PD98059. The attenuation of the cadmium-provoked apoptosis by SB203580
was a highly specific effect. In fact, the kinase inhibitor did not
prevent the generation of apoptosis by heat shock and camptothecin, nor
the generation of necrosis by cadmium treatment of glutathione-depleted
cells, nor the cadmium-provoked activation of the stress response. The generation of apoptosis was preceded by intracellular
H2O2 accumulation and was accompanied by the
disruption of mitochondrial transmembrane potential, both of which were
inhibited by SB203580. On the other hand, the antioxidant agent
butylated hydroxyanisole-inhibited apoptosis but did not prevent
p38MAPK phosphorylation. In a similar manner,
p38MAPK phosphorylation was not affected by the caspase
inhibitors Z-VAD and DEVD-CHO, which nevertheless prevented apoptosis.
These results indicate that p38MAPK activation is an early
and specific regulatory event for the cadmium-provoked apoptosis in
promonocytic cells.
Stimulation of p38 Mitogen-activated Protein Kinase Is an
Early Regulatory Event for the Cadmium-induced Apoptosis in Human
Promonocytic Cells*
§,
,§,,,**
Centro de Investigaciones Biológicas,
CSIC, 28006 Madrid, Spain and the ¶ Center for Experimental
Therapeutics and Department of Pharmacology, University of Pennsylvania
School of Medicine, Philadelphia, Pennsylvania 19104-6160
*
This work was supported by Grant PB97-0144 from the
Dirección General de Enseñanza Superior e
Investigación Científica, Grant 08.1/0027/1997 from the
Comunidad Autónoma de Madrid, Spain (to P. A.), Grant
RPG-97-092-01-CNE from the American Cancer Society, and Grant ROI-CA
74197-01 from the National Institutes of Health (to M. G. K.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Recipient of a postdoctoral fellowship from the
Fundación Ramón Areces, Spain.
**
To whom correspondence may be addressed: Centro de Investigaciones
Biológicas, CSIC, Velázquez 144, 28006 Madrid, Spain. Tel.:
34-915644562 (ext. 4247); Fax: 34-915627518; E-mail:
aller@cib.csic.es.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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