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首页> 外文期刊>Osteoarthritis and cartilage >Rac1 signaling regulates CTGF/CCN2 gene expression via TGFbeta/Smad signaling in chondrocytes.
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Rac1 signaling regulates CTGF/CCN2 gene expression via TGFbeta/Smad signaling in chondrocytes.

机译：Rac1信号传导通过软骨细胞中的TGFbeta / Smad信号传导调节CTGF​​ / CCN2基因表达。

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OBJECTIVE: Connective tissue growth factor (CTGF) has been implicated in regulation of chondrocyte differentiation at multiple steps and has been implicated in the progression of diseases such as scleroderma and osteoarthritis. However, the pathways mediating the expression of CTGF/CCN2 and related factors in cartilage are not fully understood. We have previously shown that the Rho family of proteins and the actin cytoskeleton regulate both early and late chondrocyte differentiation. RESULTS: Here we demonstrate that several CTGF/Cyr61/Nov (CCN) family members are differentially affected by either inhibition of actin polymerization (cytochalasin D treatment), promotion of actin polymerization (jasplakinolide treatment), inhibition of RhoA/rho kinase (ROCK) signaling (Y27632 treatment) and Rac1 signaling. We also show that the Smad site in the CTGF/CCN2 promoter is responsive to both Rac1 inhibition and cytochalasin D treatment, suggesting a role of TGFbeta/Smad signaling in mediating the effects of actin dynamics and Rac1. CONCLUSION: Collectively, these data show that Rac1 and actin pathways control CTGF/CCN2 expression in chondrocytes which might be relevant to both skeletal development and associated diseases such as osteoarthritis.
机译：目的：结缔组织生长因子（CTGF）与软骨细胞分化的调控有关，并与硬皮病和骨关节炎等疾病的发展有关。然而，介导CTGF / CCN2和相关因子在软骨中表达的途径尚不完全清楚。先前我们已经表明，Rho蛋白家族和肌动蛋白细胞骨架可调节早期和晚期软骨细胞分化。结果：在这里我们证明了几个CTGF / Cyr61 / Nov（CCN）家族成员受到肌动蛋白聚合的抑制（细胞松弛素D处理），肌动蛋白聚合的促进（雅斯普利奈德处理），RhoA / rho激酶（ROCK）的抑制而受到不同的影响。信号（Y27632处理）和Rac1信号。我们还显示，CTGF / CCN2启动子中的Smad位点对Rac1抑制和细胞松弛素D处理均具有响应性，表明TGFbeta / Smad信号传导在介导肌动蛋白动力学和Rac1的作用中发挥作用。结论：这些数据表明，Rac1和肌动蛋白通路控制着软骨细胞中CTGF / CCN2的表达，这可能与骨骼发育及相关疾病如骨关节炎有关。

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