ArticlePloS one2016
Antagonistic Functions of USAG-1 and RUNX2 during Tooth Development.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 74 citations in OpenAlex.
- Stem cells in regenerative dentistry: Current understanding and future directions.Journal of oral biosciences · 2024Review
- Sostdc1 Suppression in the Absence of Sclerostin Potentiates Anabolic Action of Cortical Bone in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Advances in tooth agenesis and tooth regeneration.Regenerative therapy · 2023Review
- Identification of a familial cleidocranial dysplasia with a novel RUNX2 mutation and establishment of patient-derived induced pluripotent stem cells.Odontology · 2022Article
- Role of Sostdc1 in skeletal biology and cancer.Frontiers in physiology · 2022Review
- Local application of Usag-1 siRNA can promote tooth regeneration in Runx2-deficient mice.Scientific reports · 2021Article
- Anti-USAG-1 therapy for tooth regeneration through enhanced BMP signaling.Science advances · 2021Article
- Development of tooth regenerative medicine strategies by controlling the number of teeth using targeted molecular therapy.Inflammation and regeneration · 2020Review
- Wnt Antagonists in Hematopoietic and Immune Cell Fate: Implications for Osteoporosis Therapies.Current osteoporosis reports · 2019Review
- SOSTDC1 inhibits bone metastasis in non-small cell lung cancer and may serve as a clinical therapeutic target.International journal of molecular medicine · 2018Article
- Loss of Stemness, EMT, and Supernumerary Tooth Formation in CebpbScientific reports · 2018Article
- Supernumerary teeth: A pictorial review and revised classification.Journal of oral biology and craniofacial researchReview
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Supernumerary teeth and tooth agenesis are common morphological anomalies in humans. We previously obtained evidence that supernumerary maxillary incisors form as a result of the successive development of the rudimentary maxillary incisor tooth germ in Usag-1 null mice. The development of tooth germs is arrested in Runx2 null mice, and such mice also exhibit lingual epithelial buds associated with the upper molars and incisors. The aim of this study is to investigate the potential crosstalk between Usag-1 and Runx2 during tooth development. In the present study, three interesting phenomena were observed in double null Usag-1-/-/Runx2-/- mice: the prevalence of supernumerary teeth was lower than in Usag-1 null mice; tooth development progressed further compared than in Runx2 null mice; and the frequency of molar lingual buds was lower than in Runx2 null mice. Therefore, we suggest that RUNX2 and USAG-1 act in an antagonistic manner. The lingual bud was completely filled with odontogenic epithelial Sox2-positive cells in the Usag-1+/+/Runx2-/- mice, whereas almost no odontogenic epithelial Sox2-positive cells contributed to supernumerary tooth formation in the rudimentary maxillary incisors of the Usag-1-/-/Runx2+/+ mice. Our findings suggest that RUNX2 directly or indirectly prevents the differentiation and/or proliferation of odontogenic epithelial Sox2-positive cells. We hypothesize that RUNX2 inhibits the bone morphogenetic protein (BMP) and/or Wnt signaling pathways regulated by USAG-1, whereas RUNX2 expression is induced by BMP signaling independently of USAG-1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.