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dc.contributor.authorDuncan, H.F.
dc.contributor.authorKobayashi, Y.
dc.contributor.authorYamauchi, Y.
dc.contributor.authorQuispe-Salcedo, A.
dc.contributor.authorChao Feng, Z.
dc.contributor.authorHuang, J.
dc.contributor.authorPartridge, N.C.
dc.contributor.authorNakatani, T.
dc.contributor.authorD’Armiento, J.
dc.contributor.authorShimizu, E.
dc.date.accessioned2025-10-31T18:34:13Z
dc.date.available2025-10-31T18:34:13Z
dc.date.issued2022
dc.identifier.urihttps://hdl.handle.net/20.500.12805/5094
dc.description.abstractMatrix-metalloproteinase-13 (MMP13) is important for bone formation and remodeling; however, its role in tooth development remains unknown. To investigate this, MMP13-knockout (Mmp13−/−) mice were used to analyze phenotypic changes in the dentin–pulp complex, mineralization-associated marker-expression, and mechanistic interactions. Immunohistochemistry demonstrated high MMP13-expression in pulp-tissue, ameloblasts, odontoblasts, and dentin in developing WT-molars, which reduced in adults, with human-DPC cultures demonstrating a >2000-fold increase in Mmp13-expression during mineralization. Morphologically, Mmp13−/− molars displayed critical alterations in the dentin-phenotype, affecting dentin-tubule regularity, the odontoblast-palisade and predentin-definition with significantly reduced dentin volume (∼30% incisor; 13% molar), and enamel and dentin mineral-density. Reactionary-tertiary-dentin in response to injury was reduced at Mmp13−/− molar cusp-tips but with significantly more dystrophic pulpal mineralization in MMP13-null samples. Odontoblast differentiation-markers, nestin and DSP, reduced in expression after MMP13-loss in vivo, with reduced calcium deposition in MMP13-null DPC cultures. RNA-sequencing analysis of WT and Mmp13−/− pulp highlighted 5,020 transcripts to have significantly >2.0-fold change, with pathway-analysis indicating downregulation of the Wnt-signaling pathway, supported by reduced in vivo expression of the Wnt-responsive gene Axin2. Mmp13 interaction with Axin2 could be partly responsible for the loss of odontoblastic activity and alteration to the tooth phenotype and volume which is evident in this study. Overall, our novel findings indicate MMP13 as critical for tooth development and mineralization processes, highlighting mechanistic interaction with the Wnt-signaling pathway.en_US
dc.description.sponsorshipThis study was supported in ES’s laboratory by a grant from the National Institutes of Dental and Craniofacial Research (NIDCR) R01-DE025885 and a NIH grant for microCT equipment -S10 OD010751. HD was supported by a research fellowship awarded by the European Molecular Biology Organization (EMBO) ASTF 167-2016.
dc.formatapplication/pdf
dc.language.isoeng
dc.publisherFrontiers Media
dc.relation.ispartofurn:issn:2296-634X
dc.rightshttps://purl.org/coar/access_right/c_abf2
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/
dc.subjectEndodontics and Dental Regenerationen_US
dc.subjectCellular Mechanisms in Dental Pulp Regenerationen_US
dc.titleThe Critical Role of MMP13 in Regulating Tooth Development and Reactionary Dentinogenesis Repair Through the Wnt Signaling Pathwayen_US
dc.typehttps://purl.org/coar/resource_type/c_2df8fbb1
dc.identifier.doihttps://doi.org/10.3389/fcell.2022.883266
dc.subject.ocdehttps://purl.org/pe-repo/ocde/ford#3.02.14
dc.type.otherResearch article
dc.identifier.journalFrontiers in Cell and Developmental Biology
dc.type.versionhttps://purl.org/coar/version/c_970fb48d4fbd8a85


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