MicroRNA-29 Family Suppresses Mineralization in Dental Follicle Cells

DOI Web Site 参考文献23件
  • Tomoki Risa
    Department of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo
  • Ogura Naomi
    Department of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo
  • Takahashi Kosuke
    Department of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo
  • Ito Ko
    Department of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo
  • Kondoh Toshirou
    Department of Maxillofacial Surgery, Nihon University School of Dentistry at Matsudo Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo

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The dental follicle is an ectomesenchymal tissue surrounding developing tooth germ, and contains osteoblastic-lineage-committed stem/progenitor cells. MicroRNA (miRNAs) are small non-coding RNAs that regulate gene expression during stem cell growth, proliferation and differentiation. The aim of this study is to investigate the key regulators of miRNA during osteogenic differentiation in hDFC. We therefore analyzed miRNA expression profiles in hDFC during osteoblastic differentiation. Expression of miR-29a, -29b and 29c decreased in hDFC during osteogenic induction on microarray analysis. Real-time RT-PCR analysis also showed that the expression of miR-29 family members was significantly decreased in hDFC during osteogenic differentiation. The miR-29 family was predicted to target collagen type I alpha 1 and alpha 2 by in silico analysis. When miR-29s were transfected into hDFC, collagen type I production decreased. In addition, hDFC transfected with miR-29 mimics showed delayed mineralization when compared to hDFC transfected with negative control and nontrasfection culture. Our data suggest that miR-29 negatively regulates the osteogenic differentiation/mineralization of hDFC by targeting collagen type I.

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