論文

査読有り
2020年3月

microRNA-875-5p plays critical role for mesenchymal condensation in epithelial-mesenchymal interaction during tooth development

Scientific Reports
  • Keita Funada
  • Keigo Yoshizaki
  • Kanako MIyazaki
  • Xue Han
  • Tomomi Yuta
  • Tian Tian
  • Kanji Mizuta
  • Yao Fu
  • Tsutomu Iwamoto
  • Aya Yamada
  • Ichiro Takahashi
  • Satoshi Fukumoto
  • 全て表示

10
1
記述言語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41598-020-61693-w
出版者・発行元
Springer Science and Business Media LLC

<title>Abstract</title>Epithelial-mesenchymal interaction has critical roles for organ development including teeth, during which epithelial thickening and mesenchymal condensation are initiated by precise regulation of the signaling pathway. In teeth, neural crest-derived mesenchymal cells expressed PDGF receptors migrate and become condensed toward invaginated epithelium. To identify the molecular mechanism of this interaction, we explored the specific transcriptional start sites (TSSs) of tooth organs using cap analysis of gene expression (CAGE). We identified a tooth specific TSS detected in the chromosome 15qD1 region, which codes microRNA-875 (mir875). MiR875-5p is specifically expressed in dental mesenchyme during the early stage of tooth development. Furthermore, PRRX1/2 binds to the mir875 promoter region and enhances the expression of mir875. To assess the role of miR875-5p in dental mesenchyme, we transfected mimic miR875-5p into mouse dental pulp (mDP) cells, which showed that cell migration toward dental epithelial cells was significantly induced by miR875-5p via the PDGF signaling pathway. Those results also demonstrated that miR875-5p induces cell migration by inhibiting PTEN and STAT1, which are regulated by miR875-5p as part of post-transcriptional regulation. Together, our findings indicate that tooth specific miR875-5p has important roles in cell condensation of mesenchymal cells around invaginated dental epithelium and induction of epithelial-mesenchymal interaction.

リンク情報
DOI
https://doi.org/10.1038/s41598-020-61693-w
URL
http://www.nature.com/articles/s41598-020-61693-w.pdf
URL
http://www.nature.com/articles/s41598-020-61693-w
ID情報
  • DOI : 10.1038/s41598-020-61693-w
  • eISSN : 2045-2322

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