CCN3-mediated promotion of sulfated proteoglycan synthesis in rat chondrocytes from developing joint heads
CCN3-mediated promotion of sulfated proteoglycan synthesis in rat chondrocytes from developing joint heads
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DOI：
10.1007/s12079-011-0135-1
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发表时间：
2011-08-01
影响因子：
4.1
通讯作者：
Takigawa, Masaharu
中科院分区：
文献类型：
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作者：
Janune, Danilo;Kubota, Satoshi;Takigawa, Masaharu
形成关节软骨的软骨细胞包埋在大量的细胞外基质中，所述细胞外基质具有物理刚度和弹性，所述物理刚度和弹性是支撑来自骨的机械负荷并使滑膜关节能够灵活运动的性质。与通过形成生长板来引导长骨生长的软骨细胞不同，关节软骨细胞显示抑制的细胞增殖，除非这些细胞暴露于病理条件如机械过载。在本研究中，我们发现CCN家族的成员之一，CCN 3，在发育中的大鼠滑膜关节的骨骺头分离的软骨细胞中显着表达。重组CCN 3对这些软骨细胞的影响的评估显示，CCN 3促进蛋白多糖的合成，而该因子抑制相同细胞的增殖。这些结果表明CCN 3在调节关节软骨细胞生物学特性方面发挥着关键作用。
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.