Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-5760
Authors: Imhof, Thomas
Rosenblatt, Katharina
Pryymachuk, Galyna
Weiland, Daniela
Noetzel, Nicolas
Deschner, James
Baris, Olivier R.
Kimoloi, Sammy
Koch, Manuel
Wiesner, Rudolf J.
Korkmaz, Yüksel
Title: Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
Online publication date: 23-Apr-2021
Year of first publication: 2020
Language: english
Abstract: The formation of dentin and enamel matrix depends on reciprocal interactions between epithelial-mesenchymal cells. To assess the role of mitochondrial function in amelogenesis and dentinogenesis, we studied postnatal incisor development in K320E-TwinkleEpi mice. In these mice, a loss of mitochondrial DNA (mtDNA), followed by a severe defect in the oxidative phosphorylation system is induced specifically in Keratin 14 (K14+) expressing epithelial cells. Histochemical staining showed severe reduction of cytochrome c oxidase activity only in K14+ epithelial cells. In mutant incisors, H&E staining showed severe defects in the ameloblasts, in the epithelial cells of the stratum intermedium and the papillary cell layer, but also a disturbed odontoblast layer. The lack of amelogenin in the enamel matrix of K320E-TwinkleEpi mice indicated that defective ameloblasts are not able to form extracellular enamel matrix proteins. In comparison to control incisors, von Kossa staining showed enamel biomineralization defects and dentin matrix impairment. In mutant incisor, TUNEL staining and ultrastructural analyses revealed differentiation defects, while in hair follicle cells apoptosis is prevalent. We concluded that mitochondrial oxidative phosphorylation in epithelial cells of the developed incisor is required for Ca2+ homeostasis to regulate the formation of enamel matrix and induce the differentiation of ectomesenchymal cells into odontoblasts.
DDC: 610 Medizin
610 Medical sciences
Institution: Johannes Gutenberg-Universität Mainz
Department: FB 04 Medizin
Place: Mainz
ROR: https://ror.org/023b0x485
DOI: http://doi.org/10.25358/openscience-5760
Version: Published version
Publication type: Zeitschriftenaufsatz
License: CC BY
Information on rights of use: https://creativecommons.org/licenses/by/4.0/
Journal: Scientific reports
10
Pages or article number: 22037
Publisher: Macmillan Publishers Limited, part of Springer Nature
Publisher place: London
Issue date: 2020
ISSN: 2045-2322
Publisher URL: https://doi.org/10.1038/s41598-020-77954-7
Publisher DOI: 10.1038/s41598-020-77954-7
Appears in collections:JGU-Publikationen

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