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J. Biol. Chem., Vol. 276, Issue 46, 43320-43327, November 16, 2001
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From the Neural progenitor cells (NPC) can proliferate,
differentiate into neurons or glial cells, or undergo a form of
programmed cell death called apoptosis. Although death of NPC occurs
during development of the nervous system and in the adult, the
underlying mechanisms are unknown. Here we show that nitric oxide (NO)
can induce death of C17.2 NPC by a mechanism requiring activation of
p38 MAP kinase, poly(ADP-ribose) polymerase, and caspase-3. Nitric
oxide causes release of cytochrome c from mitochondria, and
Bcl-2 protects the neural progenitor cells against nitric oxide-induced
death, consistent with a pivotal role for mitochondrial changes in
controlling the cell death process. Inhibition of p38 MAP kinase by
SB203580 abolished NO-induced cell death, cytochrome c
release, and activation of caspase-3, indicating that p38 activation serves as an upstream mediator in the cell death process. The anti-apoptotic protein Bcl-2 protected NPC against nitric oxide-induced apoptosis and suppressed activation of p38 MAP kinase. The ability of nitric oxide to trigger death of NPC by a mechanism involving p38
MAP kinase suggests that this diffusible gas may regulate NPC fate in
physiological and pathological settings in which NO is produced.
p38 MAP Kinase Mediates Nitric Oxide-induced
Apoptosis of Neural Progenitor Cells*
,,,, and§¶
Laboratory of Neurosciences, National
Institute on Aging Gerontology Research Center, Baltimore, Maryland
21224 and the § Department of Neuroscience, Johns Hopkins
University School of Medicine, Baltimore, Maryland 21205
*
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.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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