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Originally published In Press as doi:10.1074/jbc.M205193200 on June 4, 2002

J. Biol. Chem., Vol. 277, Issue 33, 30375-30381, August 16, 2002
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p38 Kinase-dependent and -independent Inhibition of Protein Kinase C zeta  and -alpha Regulates Nitric Oxide-induced Apoptosis and Dedifferentiation of Articular Chondrocytes*

Song-Ja KimDagger , Han-Gyul Kim, Chun-Do Oh, Sang-Gu Hwang, Woo-Keun Song§, Yung-Joon Yoo, Shin-Sung Kang, and Jang-Soo Chun||

From the Department of Life Science, Kwangju Institute of Science and Technology, Gwangju 500-712, Korea and the  Department of Biology, Kyungpook National University, Daegu 702-701, Korea

In articular chondrocytes, nitric oxide (NO) production triggers dedifferentiation and apoptotic cell death that is regulated by the converse functions of two mitogen-activated protein kinase subtypes, extracellular signal-regulated kinase (ERK) and p38 kinase. Since protein kinase C (PKC) transduces signals that influence differentiation, survival, and apoptosis of various cell types, we investigated the roles and underlying molecular mechanisms of action of PKC isoforms in NO-induced dedifferentiation and apoptosis of articular chondrocytes. We report here that among the expressed isoforms, activities of PKCalpha and -zeta were reduced during NO-induced dedifferentiation and apoptosis. Inhibition of PKCalpha activity was independent of NO-induced activation of ERK or p38 kinase and occurred due to blockage of expression. On the other hand, PKCzeta activity was inhibited as a result of NO-induced p38 kinase activation and was observed prior to proteolytic cleavage by a caspase-mediated process to generate enzymatically inactive fragments. Inhibition of PKCalpha or -zeta activities potentiated NO-induced apoptosis, whereas ectopic expression of these isoforms significantly reduced the number of apoptotic cells and blocked dedifferentiation. Ectopic expression of PKCalpha or -zeta did not affect p38 kinase or ERK but inhibited the p53 accumulation and caspase-3 activation that are required for NO-induced apoptosis of chondrocytes. Therefore, our results collectively indicate that p38 kinase-independent and -dependent inhibition of PKCalpha and -zeta , respectively, regulates NO-induced apoptosis and dedifferentiation of articular chondrocytes.

* This work was supported by the National Research Laboratory Program (Grant M1-0104-00-0064) and the Science Research Center for Control of Nitric Oxide Radical Toxicity.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.

Dagger Funded by a grant from the Brain Korea 21 Program.

§ Funded by a grant from the Korea Ministry of Science and Technology (Life Phenomena and Function Research Group).

|| To whom correspondence should be addressed: Department 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.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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