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Rho activation is required for transforming growth factor‐β‐induced epithelial‐mesenchymal transition in lens epithelial cells
Author(s) -
Cho Hee Jun,
Yoo Jiyun
Publication year - 2007
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2007.04.006
Subject(s) - epithelial–mesenchymal transition , transforming growth factor , microbiology and biotechnology , lens (geology) , chemistry , actin , effector , in vivo , signal transduction , rho associated protein kinase , protein kinase b , downregulation and upregulation , biology , cancer research , biochemistry , gene , paleontology
Lens epithelial cells undergo epithelial‐mesenchymal transition (EMT) after injury as in cataract extraction, leading to fibrosis of the lens capsule. We have recently shown that TGF‐β‐induced EMT in lens epithelial cells depends on PI3 kinase/Akt signal pathway. In this report, we suggest Smad3 is necessary for TGF‐β‐induced EMT by showing that the expression of dominant‐negative Smad3 blocks the expression of α‐smooth muscle actin (α‐SMA) and morphological changes. We also show that TGF‐β induces a biphasic change in Rho activity, and that Y27632, a selective inhibitor of Rho effector ROCK, inhibits TGF‐β‐induced EMT in vitro and in vivo . We finally show that Smad3 activation and Rho signal activation is independent each other. All of these findings suggest that Rho/ROCK activation together with Smad3 is necessary for TGF‐β‐induced EMT in lens epithelial cells.