Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor

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 mit...

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Autores principales: Thomas Imhof, Katharina Rosenblatt, Galyna Pryymachuk, Daniela Weiland, Nicolas Noetzel, James Deschner, Olivier R. Baris, Sammy Kimoloi, Manuel Koch, Rudolf J. Wiesner, Yüksel Korkmaz
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Publicado: Nature Portfolio 2020
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spelling oai:doaj.org-article:f049116023de4f6289ee1a5fc21019492021-12-02T12:42:27ZEpithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor10.1038/s41598-020-77954-72045-2322https://doaj.org/article/f049116023de4f6289ee1a5fc21019492020-12-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-77954-7https://doaj.org/toc/2045-2322Abstract 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.Thomas ImhofKatharina RosenblattGalyna PryymachukDaniela WeilandNicolas NoetzelJames DeschnerOlivier R. BarisSammy KimoloiManuel KochRudolf J. WiesnerYüksel KorkmazNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-11 (2020)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Thomas Imhof
Katharina Rosenblatt
Galyna Pryymachuk
Daniela Weiland
Nicolas Noetzel
James Deschner
Olivier R. Baris
Sammy Kimoloi
Manuel Koch
Rudolf J. Wiesner
Yüksel Korkmaz
Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
description 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.
format article
author Thomas Imhof
Katharina Rosenblatt
Galyna Pryymachuk
Daniela Weiland
Nicolas Noetzel
James Deschner
Olivier R. Baris
Sammy Kimoloi
Manuel Koch
Rudolf J. Wiesner
Yüksel Korkmaz
author_facet Thomas Imhof
Katharina Rosenblatt
Galyna Pryymachuk
Daniela Weiland
Nicolas Noetzel
James Deschner
Olivier R. Baris
Sammy Kimoloi
Manuel Koch
Rudolf J. Wiesner
Yüksel Korkmaz
author_sort Thomas Imhof
title Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
title_short Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
title_full Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
title_fullStr Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
title_full_unstemmed Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
title_sort epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
publisher Nature Portfolio
publishDate 2020
url https://doaj.org/article/f049116023de4f6289ee1a5fc2101949
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