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Article: Constitutive activation of β-catenin in ameloblasts leads to incisor enamel hypomineralization

TitleConstitutive activation of β-catenin in ameloblasts leads to incisor enamel hypomineralization
Authors
Keywordsβ-Catenin
Ameloblast
Enamel
Hypomineralization
Issue Date2018
PublisherSpringer Verlag Dordrecht. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1567-2379
Citation
Journal of Molecular Histology, 2018, v. 49 n. 5, p. 499-507 How to Cite?
AbstractEnamel is the hardest tissue with the highest degree of mineralization protecting the dental pulp from injury in vertebrates. The ameloblasts differentiated from ectoderm-derived epithelial cells are a single cell layer and are important for the enamel formation and mineralization. Wnt/β-catenin signaling has been proven to exert an important role in the mineralization of bone, dentin and cementum. Little was known about the regulatory mechanism of Wnt/β-catenin signaling pathway in ameloblasts during amelogenesis, especially in the mineralization of enamel. To investigate the role of β-catenin in ameloblasts, we established Amelx-Cre; β-catenin∆ex3fl/fl (CA-β-catenin) mice, which could constitutive activate β-catenin in ameloblasts. It showed the delayed mineralization and eventual hypomineralization in the incisor enamel of CA-β-catenin mice. Meanwhile, the amelogenesis-related proteinases Mmp20 and Klk4 were decreased in the incisors of CA-β-catenin mice. These data indicated that β-catenin plays an essential role in differentiation and function of ameloblasts during amelogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/279122
ISSN
2017 Impact Factor: 2.412
2015 SCImago Journal Rankings: 0.755

 

DC FieldValueLanguage
dc.contributor.authorFan, L-
dc.contributor.authorDeng, S-
dc.contributor.authorSui, X-
dc.contributor.authorLiu, M-
dc.contributor.authorCheng, S-
dc.contributor.authorWang, Y-
dc.contributor.authorGao, Y-
dc.contributor.authorChu, CH-
dc.contributor.authorZhang, Q-
dc.date.accessioned2019-10-21T02:19:58Z-
dc.date.available2019-10-21T02:19:58Z-
dc.date.issued2018-
dc.identifier.citationJournal of Molecular Histology, 2018, v. 49 n. 5, p. 499-507-
dc.identifier.issn1567-2379-
dc.identifier.urihttp://hdl.handle.net/10722/279122-
dc.description.abstractEnamel is the hardest tissue with the highest degree of mineralization protecting the dental pulp from injury in vertebrates. The ameloblasts differentiated from ectoderm-derived epithelial cells are a single cell layer and are important for the enamel formation and mineralization. Wnt/β-catenin signaling has been proven to exert an important role in the mineralization of bone, dentin and cementum. Little was known about the regulatory mechanism of Wnt/β-catenin signaling pathway in ameloblasts during amelogenesis, especially in the mineralization of enamel. To investigate the role of β-catenin in ameloblasts, we established Amelx-Cre; β-catenin∆ex3fl/fl (CA-β-catenin) mice, which could constitutive activate β-catenin in ameloblasts. It showed the delayed mineralization and eventual hypomineralization in the incisor enamel of CA-β-catenin mice. Meanwhile, the amelogenesis-related proteinases Mmp20 and Klk4 were decreased in the incisors of CA-β-catenin mice. These data indicated that β-catenin plays an essential role in differentiation and function of ameloblasts during amelogenesis.-
dc.languageeng-
dc.publisherSpringer Verlag Dordrecht. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1567-2379-
dc.relation.ispartofJournal of Molecular Histology-
dc.rightsThis is a post-peer-review, pre-copyedit version of an article published in [insert journal title]. The final authenticated version is available online at: http://dx.doi.org/[insert DOI]-
dc.subjectβ-Catenin-
dc.subjectAmeloblast-
dc.subjectEnamel-
dc.subjectHypomineralization-
dc.titleConstitutive activation of β-catenin in ameloblasts leads to incisor enamel hypomineralization-
dc.typeArticle-
dc.identifier.emailChu, CH: chchu@hku.hk-
dc.identifier.authorityChu, CH=rp00022-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10735-018-9788-x-
dc.identifier.pmid30066216-
dc.identifier.scopuseid_2-s2.0-85052058220-
dc.identifier.hkuros307234-
dc.identifier.volume49-
dc.identifier.issue5-
dc.identifier.spage499-
dc.identifier.epage507-
dc.publisher.placeNetherlands-

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