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doi: 10.1242/10.1242/dev.00110
DEVELOPMENT AND DISEASE |
1 Department of Life Science, Kwangju Institute of Science and Technology,
Gwangju 500-712, Korea
2 Department of Orthopaedic Surgery, Wonkwang University School of Medicine,
Iksan 570-711, Korea
3 Laboratory of Developmental Biology and Genomics, College of Veterinary
Medicine, Seoul National University, Seoul, Korea
4 TG Biotech, Kyungpook National University, Daegu 702-701, Korea
Author for correspondence (e-mail: jschun{at}kjist.ac.kr)
Accepted 14 August 2002
ß-Catenin regulates important biological processes, including embryonic development and tumorigenesis. We have investigated the role of ß-catenin in the regulation of the chondrocyte phenotype. Expression of ß-catenin was high in prechondrogenic mesenchymal cells, but significantly decreased in differentiated chondrocytes both in vivo and in vitro. Accumulation of ß-catenin by the inhibition of glycogen synthase kinase-3ß with LiCl inhibited chondrogenesis by stabilizing cell-cell adhesion. Conversely, the low level of ß-catenin in differentiated articular chondrocytes was increased by post-translational stabilization during phenotypic loss caused by a serial monolayer culture or exposure to retinoic acid or interleukin-1ß. Ectopic expression of ß-catenin or inhibition of ß-catenin degradation with LiCl or proteasome inhibitor caused de-differentiation of chondrocytes. Transcriptional activation of ß-catenin by its nuclear translocation was sufficient to cause phenotypic loss of differentiated chondrocytes. Expression pattern of Jun, a known target gene of ß-catenin, is essentially the same as that of ß-catenin both in vivo and in vitro suggesting that Jun and possibly activator protein 1 is involved in the ß-catenin regulation of the chondrocyte phenotype.
Key words: Cartilage, Chondrocytes, Differentiation, De-differentiation, ß-Catenin, Chick
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