Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-5760
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dc.contributor.authorImhof, Thomas-
dc.contributor.authorRosenblatt, Katharina-
dc.contributor.authorPryymachuk, Galyna-
dc.contributor.authorWeiland, Daniela-
dc.contributor.authorNoetzel, Nicolas-
dc.contributor.authorDeschner, James-
dc.contributor.authorBaris, Olivier R.-
dc.contributor.authorKimoloi, Sammy-
dc.contributor.authorKoch, Manuel-
dc.contributor.authorWiesner, Rudolf J.-
dc.contributor.authorKorkmaz, Yüksel-
dc.date.accessioned2021-04-23T07:49:12Z-
dc.date.available2021-04-23T07:49:12Z-
dc.date.issued2020-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/5769-
dc.description.abstractThe 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.de_DE
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleEpithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisoren_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-5760-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleScientific reportsde
jgu.journal.volume10de
jgu.pages.alternative22037de
jgu.publisher.year2020-
jgu.publisher.nameMacmillan Publishers Limited, part of Springer Naturede
jgu.publisher.placeLondonde
jgu.publisher.urihttps://doi.org/10.1038/s41598-020-77954-7de
jgu.publisher.issn2045-2322de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1038/s41598-020-77954-7
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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