Kim Dongkyun, Kim Jungsoo, Kang Shin-Sung, Jin Eun-Jung
Department of Biological Sciences, Wonkwang University, Iksan, Chunbuk, South Korea.
J Cell Biochem. 2009 Jul 1;107(4):622-9. doi: 10.1002/jcb.22191.
Endochondral ossification is characterized by a significant interdependence between cell shape and cytoskeletal organization that accompanies the onset of chondrogenic signaling. However, the mechanisms mediating these interactions have not been well studied. Here, treatment with transforming growth factor (TGF)-beta3 at a later stage of chondrogenesis led to activation of Smad-2 signaling and the formation of intense stress fibers, which resulted in suppressing chondrogenic differentiation of leg bud mesenchymal cells. Moreover, specific siRNA knockdown of Smad-2 reduced TGF-beta3-induced stress fibers via physical interactions with beta-catenin. In conclusion, our results indicate that TGF-beta3-induced Smad signaling, in conjunction with beta-catenin, is involved in the reorganization of the actin cytoskeleton into a cortical pattern with a concomitant rounding of cells. J. Cell. Biochem. (c) 2009 Wiley-Liss, Inc.This article was published online on 28 May 2009. An error was subsequently identified. This notice is included in the online and print versions to indicate that both have been corrected 8 June 2009.
软骨内骨化的特征是在软骨形成信号开始时,细胞形状与细胞骨架组织之间存在显著的相互依存关系。然而,介导这些相互作用的机制尚未得到充分研究。在此,在软骨形成后期用转化生长因子(TGF)-β3处理导致Smad-2信号激活和强烈应力纤维的形成,这导致抑制腿芽间充质细胞的软骨形成分化。此外,Smad-2的特异性小干扰RNA(siRNA)敲低通过与β-连环蛋白的物理相互作用减少了TGF-β3诱导的应力纤维。总之,我们的结果表明,TGF-β3诱导的Smad信号与β-连环蛋白一起参与了肌动蛋白细胞骨架重组成皮质模式并伴随细胞变圆的过程。《细胞生物化学杂志》(c)2009威利-利斯出版公司。本文于2009年5月28日在线发表。随后发现一个错误。本通知包含在在线版和印刷版中,以表明两者均已于2009年6月8日更正。