Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
Autor: | Imhof, Thomas, Rosenblatt, Katharina, Pryymachuk, Galyna, Weiland, Daniela, Noetzel, Nicolas, Deschner, James, Baris, Olivier R., Kimoloi, Sammy, Koch, Manuel, Wiesner, Rudolf J., Korkmaz, Yüksel |
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Přispěvatelé: | Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS) |
Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
Cell biology
Physiology [SDV]Life Sciences [q-bio] Science 610 Medizin Mice Transgenic Pathogenesis Article Oxidative Phosphorylation Electron Transport Complex IV stomatognathic system 610 Medical sciences Developmental biology Animals Dental Enamel Amelogenin Epithelial Cells Mitochondria Incisor Succinate Dehydrogenase stomatognathic diseases Animals Newborn Dentin Mutation Medicine Anatomy |
Zdroj: | Scientific Reports, Vol 10, Iss 1, Pp 1-11 (2020) Scientific Reports Scientific Reports, Nature Publishing Group, 2020, 10 (1), ⟨10.1038/s41598-020-77954-7⟩ |
ISSN: | 2045-2322 |
Popis: | International audience; 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. |
Databáze: | OpenAIRE |
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