Ten-m/Odz3 regulates migration and differentiation of chondrogenic ATDC5 cells via RhoA-mediated actin reorganization

Ikuko Takano, Nobuo Takeshita, Michiko Yoshida, Daisuke Seki, Toshihito Oyanagi, Seiji Kimura, Wei Jiang, Kiyo Sasaki, Chisumi Sogi, Masayoshi Kawatsu, Teruko Yamamoto

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
JournalJournal of Cellular Physiology
DOIs
Publication statusAccepted/In press - 2020

Keywords

  • actin cytoskeleton
  • ATDC5
  • chondrogenesis
  • RhoA
  • Ten-m/Odz3

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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