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Ameloblasts require active R ho A to generate normal dental enamel
Author(s) -
Xue Hui,
Li Yong,
Everett Eric T.,
Ryan Kathleen,
Peng Li,
Porecha Rakhee,
Yan Yan,
Lucchese Anna M.,
Kuehl Melissa A.,
Pugach Megan K.,
Bouchard Jessica,
Gibson Carolyn W.
Publication year - 2013
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/eos.12059
Subject(s) - ameloblast , amelogenin , rhoa , amelogenesis , enamel paint , chemistry , microbiology and biotechnology , transgene , enamel organ , genetically modified mouse , biology , biochemistry , signal transduction , dentistry , gene , medicine
Rho A plays a fundamental role in regulation of the actin cytoskeleton, intercellular attachment, and cell proliferation. During amelogenesis, ameloblasts (which produce the enamel proteins) undergo dramatic cytoskeletal changes and the R ho A protein level is up‐regulated. Transgenic mice were generated that express a dominant‐negative R ho A transgene in ameloblasts using amelogenin gene‐regulatory sequences. Transgenic and wild‐type ( WT ) molar tooth germs were incubated with sodium fluoride ( N aF) or sodium chloride ( N aCl) in organ culture. Filamentous actin ( F ‐actin) stained with phalloidin was elevated significantly in WT ameloblasts treated with N aF compared with WT ameloblasts treated with N aCl or with transgenic ameloblasts treated with N aF, thereby confirming a block in the R hoA/Rho‐associated protein kinase ( ROCK ) pathway in the transgenic mice. Little difference in quantitative fluorescence (an estimation of fluorosis) was observed between WT and transgenic incisors from mice provided with drinking water containing N aF. We subsequently found reduced transgene expression in incisors compared with molars. Transgenic molar teeth had reduced amelogenin, E ‐cadherin, and K i67 compared with WT molar teeth. Hypoplastic enamel in transgenic mice correlates with reduced expression of the enamel protein, amelogenin, and E ‐cadherin and cell proliferation are regulated by R ho A in other tissues. Together these findings reveal deficits in molar ameloblast function when R ho A activity is inhibited.