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Targeted Overexpression of Amelotin Disrupts the Microstructure of Dental Enamel
We have previously identified amelotin (AMTN) as a novel protein expressed predominantly during the late stages of dental enamel formation, but its role during amelogenesis remains to be determined. In this study we generated transgenic mice that produce AMTN under the amelogenin (Amel) gene promote...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335167/ https://www.ncbi.nlm.nih.gov/pubmed/22539960 http://dx.doi.org/10.1371/journal.pone.0035200 |
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author | Lacruz, Rodrigo S. Nakayama, Yohei Holcroft, James Nguyen, Van Somogyi-Ganss, Eszter Snead, Malcolm L. White, Shane N. Paine, Michael L. Ganss, Bernhard |
author_facet | Lacruz, Rodrigo S. Nakayama, Yohei Holcroft, James Nguyen, Van Somogyi-Ganss, Eszter Snead, Malcolm L. White, Shane N. Paine, Michael L. Ganss, Bernhard |
author_sort | Lacruz, Rodrigo S. |
collection | PubMed |
description | We have previously identified amelotin (AMTN) as a novel protein expressed predominantly during the late stages of dental enamel formation, but its role during amelogenesis remains to be determined. In this study we generated transgenic mice that produce AMTN under the amelogenin (Amel) gene promoter to study the effect of AMTN overexpression on enamel formation in vivo. The specific overexpression of AMTN in secretory stage ameloblasts was confirmed by Western blot and immunohistochemistry. The gross histological appearance of ameloblasts or supporting cellular structures as well as the expression of the enamel proteins amelogenin (AMEL) and ameloblastin (AMBN) was not altered by AMTN overexpression, suggesting that protein production, processing and secretion occurred normally in transgenic mice. The expression of Odontogenic, Ameloblast-Associated (ODAM) was slightly increased in secretory stage ameloblasts of transgenic animals. The enamel in AMTN-overexpressing mice was much thinner and displayed a highly irregular surface structure compared to wild type littermates. Teeth of transgenic animals underwent rapid attrition due to the brittleness of the enamel layer. The microstructure of enamel, normally a highly ordered arrangement of hydroxyapatite crystals, was completely disorganized. Tomes' process, the hallmark of secretory stage ameloblasts, did not form in transgenic mice. Collectively our data demonstrate that the overexpression of amelotin has a profound effect on enamel structure by disrupting the formation of Tomes' process and the orderly growth of enamel prisms. |
format | Online Article Text |
id | pubmed-3335167 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-33351672012-04-26 Targeted Overexpression of Amelotin Disrupts the Microstructure of Dental Enamel Lacruz, Rodrigo S. Nakayama, Yohei Holcroft, James Nguyen, Van Somogyi-Ganss, Eszter Snead, Malcolm L. White, Shane N. Paine, Michael L. Ganss, Bernhard PLoS One Research Article We have previously identified amelotin (AMTN) as a novel protein expressed predominantly during the late stages of dental enamel formation, but its role during amelogenesis remains to be determined. In this study we generated transgenic mice that produce AMTN under the amelogenin (Amel) gene promoter to study the effect of AMTN overexpression on enamel formation in vivo. The specific overexpression of AMTN in secretory stage ameloblasts was confirmed by Western blot and immunohistochemistry. The gross histological appearance of ameloblasts or supporting cellular structures as well as the expression of the enamel proteins amelogenin (AMEL) and ameloblastin (AMBN) was not altered by AMTN overexpression, suggesting that protein production, processing and secretion occurred normally in transgenic mice. The expression of Odontogenic, Ameloblast-Associated (ODAM) was slightly increased in secretory stage ameloblasts of transgenic animals. The enamel in AMTN-overexpressing mice was much thinner and displayed a highly irregular surface structure compared to wild type littermates. Teeth of transgenic animals underwent rapid attrition due to the brittleness of the enamel layer. The microstructure of enamel, normally a highly ordered arrangement of hydroxyapatite crystals, was completely disorganized. Tomes' process, the hallmark of secretory stage ameloblasts, did not form in transgenic mice. Collectively our data demonstrate that the overexpression of amelotin has a profound effect on enamel structure by disrupting the formation of Tomes' process and the orderly growth of enamel prisms. Public Library of Science 2012-04-23 /pmc/articles/PMC3335167/ /pubmed/22539960 http://dx.doi.org/10.1371/journal.pone.0035200 Text en Lacruz et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Lacruz, Rodrigo S. Nakayama, Yohei Holcroft, James Nguyen, Van Somogyi-Ganss, Eszter Snead, Malcolm L. White, Shane N. Paine, Michael L. Ganss, Bernhard Targeted Overexpression of Amelotin Disrupts the Microstructure of Dental Enamel |
title | Targeted Overexpression of Amelotin Disrupts the Microstructure of Dental Enamel |
title_full | Targeted Overexpression of Amelotin Disrupts the Microstructure of Dental Enamel |
title_fullStr | Targeted Overexpression of Amelotin Disrupts the Microstructure of Dental Enamel |
title_full_unstemmed | Targeted Overexpression of Amelotin Disrupts the Microstructure of Dental Enamel |
title_short | Targeted Overexpression of Amelotin Disrupts the Microstructure of Dental Enamel |
title_sort | targeted overexpression of amelotin disrupts the microstructure of dental enamel |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335167/ https://www.ncbi.nlm.nih.gov/pubmed/22539960 http://dx.doi.org/10.1371/journal.pone.0035200 |
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