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J. Biol. Chem., Vol. 279, Issue 25, 26597-26604, June 18, 2004

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Wnt-7a Causes Loss of Differentiated Phenotype and Inhibits Apoptosis of Articular Chondrocytes via Different Mechanisms^*

Sang-Gu Hwang, Je-Hwang Ryu, Il-Chul Kim, Eek-Hoon Jho¶||, Ho-Chul Jung**, Kwonseop Kim**, Song-Ja Kim, and Jang-Soo Chun¶¶

From the Department of Life Science, Kwangju Institute of Science and Technology, Gwangju 500-712, Korea, the ^¶Department of Life Science, University of Seoul, Seoul 130-743, Korea, the ^**College of Pharmacy, Chonnam National University, Gwangju 500-757, Korea, and the Department of Biological Science, Kongju National University, Chungnam 314-701, Korea

Although regulation of chondrogenesis and cartilage development by Wnt signaling is well established, the function of Wnt in the maintenance and destruction of cartilage remains largely unknown. Here we investigated the involvement and regulatory mechanisms of Wnt signaling in cartilage destruction. We found that interleukin-1, the primary pro-inflammatory cytokine involved in cartilage destruction, induces expression of Wnt-5a and -7a in primary culture articular chondrocytes. The level of -catenin was also increased in chondrocytes of arthritic cartilage, suggesting the association of Wnt/-catenin signaling with arthritic cartilage destruction. In addition, our results show that Wnt-7a induces dedifferentiation and inhibits NO-induced apoptosis of primary culture articular chondrocytes. Wnt-7a induces dedifferentiation of articular chondrocytes by stimulating transcriptional activity of -catenin, whereas NO-induced apoptosis is inhibited via the activation of cell survival signaling, such as phosphatidylinositol 3-kinase and Akt, which block apoptotic signaling cascade. Our results collectively suggest that Wnt-7a is associated with cartilage destruction by regulating the maintenance of differentiation status and the apoptosis of articular chondrocytes via different mechanisms.

Received for publication, February 9, 2004 , and in revised form, April 5, 2004.

^* This work was supported by National Research Laboratory Program Grant M1-0104-00-0064 from the Korea Ministry of Science and Technology and Basic Research Program of the Korea Science and Engineering Foundation Grant R01-2003-000-10154-0. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

These authors contributed equally to this work.

^|| Supported by Grant CBM1-B221-001-1-0-0 from the Center for Biological Modulators of the 21st Century Frontier R&D Program, the Ministry of Science and Technology, Korea.

Supported by Molecular Medicine Research Group Program Grant M1-0160-00-0023 from the Korea Ministry of Science and Technology.

^¶¶ To whom correspondence should be addressed: Dept. of Life Science, Kwangju Institute of Science and Technology, Buk-Gu, Gwangju 500-712, Korea. E-mail: jschun{at}kjist.ac.kr.

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