Zyxin-involved actin regulation is essential in the maintenance of vinculin focal adhesion and chondrocyte differentiation status

连接蛋白参与的肌动蛋白调节对于维持连接蛋白粘着斑和软骨细胞分化状态至关重要

阅读:5
作者:Gaoming Li, Xiongbo Song, Rui Li, Li Sun, Xiaoyuan Gong, Cheng Chen, Liu Yang

Conclusions

These results demonstrate supporting evidence that in chondrocytes the level of zyxin is closely associated with the state of actin polymerization. In particular, the change of zyxin and F-actin parallels with the change of COL II and vinculin, respectively, indicating a major role of zyxin-actin interaction in the synthesis of collagen ECM and the remodelling of cytoskeleton-ECM adhesion.

Methods

Chondrocytes obtained from rabbit articular cartilage were used in this study. The expression of zyxin, actin and vinculin, as well as the extracellular matrix (ECM) protein collagen type I, II and X (COL I, II and X) of chondrocytes were compared between zyxin-knockdown group and negative control group, and between transforming growth factor-β1 (TGF-β1) treatment group and non-treatment group, respectively.

Results

Knockdown of zyxin increased the ratio of globular actin (G-actin) to filamentous actin (F-actin) of chondrocyte, which further inhibited expression of vinculin and chondrogenic marker COL II as well as hypertrophy marker COL X. On the other hand, chondrocytes treated with TGF-β1 showed an enhanced expression of F-actin, and a lower expression of zyxin compared to non-treatment group. In response to TGF-β1-induced actin polymerization, expression of vinculin and COL I was increased, while expression of COL II and aggrecan was decreased. Conclusions: These results demonstrate supporting evidence that in chondrocytes the level of zyxin is closely associated with the state of actin polymerization. In particular, the change of zyxin and F-actin parallels with the change of COL II and vinculin, respectively, indicating a major role of zyxin-actin interaction in the synthesis of collagen ECM and the remodelling of cytoskeleton-ECM adhesion.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。