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J. Biol. Chem., Vol. 277, Issue 36, 33501-33508, September 6, 2002
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From the Department of Life Science, Kwangju Institute of Science
and Technology, Gwangju 500-712, Korea, § Department of
Microbiology, Dankook University College of Medicine, Cheonan 330-714, Korea, and ¶ Department of Biology, Kyungpook National
University, Daegu 702-701, Korea
Nitric oxide (NO) during primary culture of
articular chondrocytes causes apoptosis via p38 mitogen-activated
protein kinase in association with elevation of p53 protein level,
caspase-3 activation, and differentiation status. In this study, we
characterized the molecular mechanism by which p38 kinase induces
apoptosis through activation of p53. We report here that NO-induced
activation of p38 kinase leads to activation of NF
p38 Kinase Regulates Nitric Oxide-induced Apoptosis of Articular
Chondrocytes by Accumulating p53 via NF
B-dependent
Transcription and Stabilization by Serine 15 Phosphorylation*
,
B, which in turn
induces transcription of the p53 gene. Activated p38 kinase
also physically associates and phosphorylates the serine 15 residue of
p53, which results in accumulation of p53 protein during NO-induced
apoptosis. Ectopic expression of wild-type p53 enhanced NO-induced
apoptosis, whereas expression of a dominant negative p53 blocked it,
indicating that p53 plays an essential role in NO-induced apoptosis of
chondrocytes. The increased accumulation of p53 caused expression of
Bax, a pro-apoptotic member of the Bcl-2 family that is known to cause apoptosis via release of cytochrome c and caspase
activation. These results suggest that NO-activated p38 kinase
activates p53 function in two different ways, transcriptional
activation by NFB and direct phosphorylation of p53 protein, leading
to apoptosis of articular chondrocytes.
*
This work was supported by National Research Laboratory
Program M1-0104-00-0064, Korea Research Foundation Grant
KRF-2000-015-DP0387, Korea Ministry of Science and Technology (Life
Phenomena and Function Research Group) (to J.-S. C.), and the Science
Research Center for Control of Nitric Oxide Radical Toxicity (to
S.-S. 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.
Supported by Brain Korea 21 program.
To whom correspondence should be addressed: Dept. of Life
Science, Kwangju Institute of Science and Technology Buk-Gu, Gwangju, 500-712 Korea. Tel.: 82-62-970-2497; Fax: 82-62-970-2484; E-mail: jschun@kjist.ac.kr.
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