ArticleBiochemical and biophysical research communications2021
Ezh2 knockout in mesenchymal cells causes enamel hyper-mineralization.
Article in Biochemical and biophysical research communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- KMT2D Regulates Tooth Enamel Development.Journal of dental research · 2025Article
- Role and mechanisms of histone methylation in osteogenic/odontogenic differentiation of dental mesenchymal stem cells.International journal of oral science · 2025Review
- KMT2D regulates tooth enamel development.bioRxiv : the preprint server for biology · 2024Article
- Article
- Regulation of Hydroxyapatite Nucleation In Vitro through Ameloblastin-Amelogenin Interactions.ACS biomaterials science & engineering · 2023Article
- Lysine-Specific Demethylase 1 (LSD1) epigenetically controls osteoblast differentiation.PloS one · 2022Article
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 4 countries.
Funding
Abstract
Enhancer of zeste homolog 2 (EZH2) is the catalytic core of polycomb repressive complex 2 (PRC2), which primarily methylates lysine 27 on histone H3 (H2K27me3), generating transcriptionally suppressed heterochromatin. Since EZH2 suppresses expression of genes involved in dentin formation, we examined the role of EZH2 in tooth development. Intriguingly, microCT analysis of teeth from mice with conditional Ezh2 knockout in uncommitted mesenchymal cells showed hyper-mineralization of enamel, which is produced by the epithelial-lineage cells, ameloblasts. Scanning electron microscopy analysis and nano-indentation of the incisor enamel from knockout mice revealed smaller inter-rod spaces and higher hardness compared to wild type enamel, respectively. Interestingly, expression of the calcium channel subunit gene, Orai2, was decreased compared to its competitor, Orai1, both in knockout mouse incisors and the ex vivo culture of ameloblasts with the surrounding tissues under EZH2 inhibition. Moreover, histological analysis of incisor from knockout mice showed decreased ameloblastin and expedited KLK4 expression in the ameloblasts. These observations suggest that EZH2 depletion in dental mesenchymal cells reduces enamel matrix formation and increases enamel protease activity from ameloblasts, resulting in enamel hyper-mineralization. This study demonstrates the significant role of the suppressive H3K27me3 mark for heterochromatin on enamel formation.
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Registered trials
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