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CCN3-mediated promotion of sulfated proteoglycan synthesis in rat chondrocytes from developing joint heads

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Journal of Cell Communication and Signaling Aims and scope

Abstract

Chondrocytes forming articular cartilage are embedded in a vast amount of extracellular matrix having physical stiffness and elasticity, properties that support the mechanical load from bones and enable the flexible movement of synovial joints. Unlike chondrocytes that conduct the growth of long bones by forming the growth plate, articular chondrocytes show suppressed cell proliferation, unless these cells are exposed to pathological conditions such as mechanical overload. In the present study, we found that one of the members of the CCN family, CCN3, was significantly expressed in chondrocytes isolated from the epiphyseal head in developing rat synovial joints. Evaluation of the effect of recombinant CCN3 on those chondrocytes revealed that CCN3 promoted proteoglycan synthesis, whereas this factor repressed the proliferation of the same cells. These results suggest a critical role for CCN3 in the regulation of the biological properties of articular chondrocytes.

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Acknowledgments

This work was supported by the programs Grants-in-Aid for Scientific Research (S) [to M.T.] and (C) [to S.K.] from Japan Society for the Promotion of Science, and by a research grant from Terumo Life Science Foundation [to S.K.]. D.J. is supported by a scholarship provided by the Japanese Ministry of Education, Culture, Sports, Science, and Technology. Work performed in B. Perbal's laboratory was funded by French Ministry of Education: EA1556; and by European PROTHETS (Prognosis and Therapeutic Targets of Ewing Family of Tumors, FP6 Contract 503036).

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Correspondence to Satoshi Kubota or Masaharu Takigawa.

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Janune, D., Kubota, S., Lazar, N. et al. CCN3-mediated promotion of sulfated proteoglycan synthesis in rat chondrocytes from developing joint heads. J. Cell Commun. Signal. 5, 167–171 (2011). https://doi.org/10.1007/s12079-011-0135-1

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  • DOI: https://doi.org/10.1007/s12079-011-0135-1

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