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Ten‐m/Odz3 regulates migration and differentiation of chondrogenic ATDC5 cells via RhoA‐mediated actin reorganization
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2020-09-22 , DOI: 10.1002/jcp.30058
Ikuko Takano 1 , Nobuo Takeshita 1 , Michiko Yoshida 1 , Daisuke Seki 1 , Toshihito Oyanagi 1 , Seiji Kimura 1 , Wei Jiang 1 , Kiyo Sasaki 1 , Chisumi Sogi 2 , Masayoshi Kawatsu 1 , Teruko Takano-Yamamoto 1, 3
Affiliation  

Tenascin‐like molecule major (Ten‐m)/odd Oz (Odz), a type II transmembrane molecule, is well known to modulate neural development. We have reported that Ten‐m/Odz3 is expressed in cartilaginous tissues and cells. Actin cytoskeleton and its regulator ras homolog gene family member A (RhoA) are closely associated with chondrogenesis. The present study aimed to evaluate the function and molecular mechanism of Ten‐m/Odz3 during chondrogenesis, focusing on RhoA and the actin cytoskeleton. Ten‐m/Odz3 was expressed in precartilaginous condensing mesenchyme in mouse limb buds. Ten‐m/Odz3 knockdown in ATDC5 induced actin cytoskeleton reorganization and change of cell shape through modulation of RhoA activity and FGF2 expression. Ten‐m/Odz3 knockdown suppressed ATDC5 migration and expression of genes associated with chondrogenesis, such as Sox9 and type II collagen, via RhoA. On the other hand, Ten‐m/Odz3 knockdown inhibited proliferation of ATDC5 in a RhoA‐independent manner. These findings suggest that Ten‐m/Odz3 plays an important role in early chondrogenesis regulating RhoA‐mediated actin reorganization.

中文翻译:


Ten-m/Odz3 通过 RhoA 介导的肌动蛋白重组调节软骨形成 ATDC5 细胞的迁移和分化



腱蛋白样分子主要 (Ten-m)/奇 Oz (Odz) 是一种 II 型跨膜分子,众所周知可以调节神经发育。我们报道了 Ten-m/Odz3 在软骨组织和细胞中表达。肌动蛋白细胞骨架及其调节器ras同源基因家族成员A(RhoA)与软骨形成密切相关。本研究旨在评估 Ten-m/Odz3 在软骨形成过程中的功能和分子机制,重点关注 RhoA 和肌动蛋白细胞骨架。 Ten-m/Odz3 在小鼠肢芽的软骨前浓缩间充质中表达。 ATDC5 中的 10-m/Odz3 敲除通过调节 RhoA 活性和 FGF2 表达诱导肌动蛋白细胞骨架重组和细胞形状改变。 Ten-m/Odz3 敲除通过 RhoA 抑制 ATDC5 迁移和与软骨形成相关的基因(例如 Sox9 和 II 型胶原)的表达。另一方面,Ten-m/Odz3 敲低以不依赖 RhoA 的方式抑制 ATDC5 的增殖。这些发现表明 Ten-m/Odz3 在调节 RhoA 介导的肌动蛋白重组的早期软骨形成中发挥着重要作用。
更新日期:2020-09-22
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