ArticleScientific reports2016
Abrogation of epithelial BMP2 and BMP4 causes Amelogenesis Imperfecta by reducing MMP20 and KLK4 expression.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Integrative multi-omics and bioinformatic analysis ofThe Japanese dental science review · 2026Review
- An NKX2-3/5/6 homolog is required downstream of BMP signaling to pattern the sensory-adhesive organ of a tunicate larva.PLoS genetics · 2026Article
- A novelFrontiers in physiology · 2026Article
- Prespecified dental mesenchymal cells for the making of a tooth.International journal of oral science · 2025Article
- A Chemically Defined Culture for Tooth Reconstitution.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Rogdi knockout mouse is a model for Kohlschütter-Tönz syndrome.Scientific reports · 2024Article
- Organoids from mouse molar and incisor as new tools to study tooth-specific biology and development.Stem cell reports · 2023Article
- Loss of BMP2 and BMP4 Signaling in the Dental Epithelium Causes Defective Enamel Maturation and Aberrant Development of Ameloblasts.International journal of molecular sciences · 2022Article
- Epithelial Bone Morphogenic Protein 2 and 4 Are Indispensable for Tooth Development.Frontiers in physiology · 2021Article
- Ablation of Fam20c causes amelogenesis imperfecta via inhibiting Smad dependent BMP signaling pathway.Biology direct · 2020Article
- Tooth Formation: Are the Hardest Tissues of Human Body Hard to Regenerate?International journal of molecular sciences · 2020Review
- Role of osteoprotegerin in the regulation of dental epithelial‑mesenchymal signaling during tooth development.Molecular medicine reports · 2019Article
- Persistent Wnt/β-catenin signaling in mouse epithelium induces the ectopicOrganogenesis · 2019Article
- FAM20C regulates osteoblast behaviors and intracellular signaling pathways in a cell-autonomous manner.Journal of cellular physiology · 2018Article
- Abrogation of Fam20c altered cell behaviors and BMP signaling of immortalized dental mesenchymal cells.Experimental cell research · 2018Article
- The crucial role of the TRPM7 kinase domain in the early stage of amelogenesis.Scientific reports · 2017Article
- Deletion ofFrontiers in physiology · 2017Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Amelogenesis Imperfecta (AI) can be caused by the deficiencies of enamel matrix proteins, molecules responsible for the transportation and secretion of enamel matrix components, and proteases processing enamel matrix proteins. In the present study, we discovered the double deletion of bone morphogenetic protein 2 (Bmp2) and bone morphogenetic protein 4 (Bmp4) in the dental epithelium by K14-cre resulted in hypoplastic enamel and reduced density in X-ray radiography as well as shortened enamel rods under scanning electron microscopy. Such enamel phenotype was consistent with the diagnosis of hypoplastic amelogenesis imperfecta. Histological and molecular analyses revealed that the removal of matrix proteins in the mutant enamel was drastically delayed, which was coincided with the greatly reduced expression of matrix metalloproteinase 20 (MMP20) and kallikrein 4 (KLK4). Although the expression of multiple enamel matrix proteins was down-regulated in the mutant ameloblasts, the cleavage of ameloblastin was drastically impaired. Therefore, we attributed the AI primarily to the reduction of MMP20 and KLK4. Further investigation found that BMP/Smad4 signaling pathway was down-regulated in the K14-cre;Bmp2(f/f);Bmp4(f/f)ameloblasts, suggesting that the reduced MMP20 and KLK4 expression may be due to the attenuated epithelial BMP/Smad4 signaling.
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