During embryogenesis, chondrocytes at the epiphyseal tip of long bone models give rise to articular tissue and persist through life, whereas chondrocytes in the shaft undergo hypertrophy, mineralization and apoptosis and are replaced by bone cells. It is not understood how chondrocytes undertake these alternative pathways and fates. We have been reported that C-1-1, a novel isoform of chick ets-related gene (ERG) is preferentially expressed in articular cartilage and its expression is down-regulated during maturation of chondrocytes. Over-expression of C-1-1 not only inhibits maturation of chondrocytes but also converts type X collagen positive trangient chondrocytes to tenascin-C positive permanent articular chondrocytes like cells. In developing mouse skeleton, ERG is highly expressed in future joint region and surface zone of articular cartilage. Those findings suggest that ERG plays an important role in permanent articular cartilage formation. We are studying mechanism of action, regulation of expression, interaction and interplay with other signaling factors, and the effect of down-regulation of ERG in chondrocytes.

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