Transgenic rescue of enamel phenotype in Ambn null mice

Y. H.P. Chun, Y. Lu, Y. Hu, P. H. Krebsbach, Y. Yamada, J. C.C. Hu, J. P. Simmer

Producción científica: Articlerevisión exhaustiva

22 Citas (Scopus)

Resumen

Ameloblastin null mice fail to make an enamel layer, but the defects could be due to an absence of functional ameloblastin or to the secretion of a potentially toxic mutant ameloblastin. We hypothesized that the enamel phenotype could be rescued by the transgenic expression of normal ameloblastin in Ambn mutant mice. We established and analyzed 5 transgenic lines that expressed ameloblastin from the amelogenin (AmelX) promoter and identified transgenic lines that express virtually no transgene, slightly less than normal (Tg+), somewhat higher than normal (Tg++), and much higher than normal (Tg+++) levels of ameloblastin. All lines expressing detectable levels of ameloblastin at least partially recovered the enamel phenotype. When ameloblastin expression was only somewhat higher than normal, the enamel covering the molars and incisors was of normal thickness, had clearly defined rod and interrod enamel, and held up well in function. We conclude that ameloblastin is essential for dental enamel formation.

Idioma originalEnglish (US)
Páginas (desde-hasta)1414-1420
Número de páginas7
PublicaciónJournal of dental research
Volumen89
N.º12
DOI
EstadoPublished - dic 2010

ASJC Scopus subject areas

  • General Dentistry

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