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Ten‐m/Odz3 regulates migration and differentiation of chondrogenic ATDC5 cells via RhoA‐mediated actin reorganization
Author(s) -
Takano Ikuko,
Takeshita Nobuo,
Yoshida Michiko,
Seki Daisuke,
Oyanagi Toshihito,
Kimura Seiji,
Jiang Wei,
Sasaki Kiyo,
Sogi Chisumi,
Kawatsu Masayoshi,
TakanoYamamoto Teruko
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30058
Subject(s) - rhoa , microbiology and biotechnology , gene knockdown , chondrogenesis , actin cytoskeleton , cytoskeleton , actin , biology , chemistry , signal transduction , gene , cell , mesenchymal stem cell , biochemistry
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.