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Functional role of rho‐kinase in ameloblast differentiation
Author(s) -
Otsu Keishi,
Kishigami Ryota,
Fujiwara Naoki,
Ishizeki Kiyoto,
Harada Hidemitsu
Publication year - 2011
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.22597
Subject(s) - ameloblast , amelogenin , microbiology and biotechnology , rock1 , amelogenesis , rock2 , biology , enamel organ , cellular differentiation , cell adhesion , chemistry , cell , rho associated protein kinase , kinase , protein kinase a , enamel paint , materials science , biochemistry , composite material , gene
During tooth development, inner enamel epithelial (IEE) cells differentiate into enamel‐secreting ameloblasts, a polarized and elongated cellular population. The molecular underpinnings of this morphogenesis and cytodifferentiation, however, are not well understood. Here, we show that Rho‐associated coiled‐coil‐containing protein kinase (ROCK) regulates ameloblast differentiation and enamel formation. In mouse incisor organ cultures, inhibition of ROCK, hindered IEE cell elongation and disrupted polarization of differentiated ameloblasts. Expression of enamel matrix proteins, such as amelogenin and ameloblastin, and formation of the terminal band structure of actin and E‐cadherin were also perturbed. Cultures of dental epithelial cells revealed that ROCK regulates cell morphology and cell adhesion through localization of actin bundles, E‐cadherin, and β‐catenin to cell membranes. Moreover, inhibition of ROCK promoted cell proliferation. Small interfering RNA specific for ROCK1 and ROCK2 demonstrated that the ROCK isoforms performed complementary functions in the regulation of actin organization and E‐cadherin‐mediated cell–cell adhesion. Thus, our results have uncovered a novel role for ROCK in amelogenesis. J. Cell. Physiol. 226: 2527–2534, 2011. © 2010 Wiley‐Liss, Inc.

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