Intracellular Signaling Pathway Activation via TGF-β Differs in the Anterior and Posterior Axis During Palatal Development

• Higa Arisa

  Section of Pediatric Dentistry, Department of Oral Growth and Development, Fukuoka Dental College

• Oka Kyoko

  Section of Pediatric Dentistry, Department of Oral Growth and Development, Fukuoka Dental College

• Kira-Tatsuoka Michiko

  Section of Pediatric Dentistry, Department of Oral Growth and Development, Fukuoka Dental College

• Tamura Shougo

  Section of Pediatric Dentistry, Department of Oral Growth and Development, Fukuoka Dental College

• Itaya Satoshi

  Section of Pediatric Dentistry, Department of Oral Growth and Development, Fukuoka Dental College

• Toda Masako

  Section of Pediatric Dentistry, Department of Oral Growth and Development, Fukuoka Dental College

• Ozaki Masao

  Section of Pediatric Dentistry, Department of Oral Growth and Development, Fukuoka Dental College

• Sawa Yoshihiko

  Section of Functional Structure, Department of Morphological Biology, Division of Biomedical Sciences, Fukuoka Dental College

抄録

It is important to understand the different mechanisms involved in anterior hard and posterior soft palate development to prevent and treat patients with cleft palate. Genetic analyses of humans and gene-mutated mice with cleft palate have shown that TGF-β signaling has a critical role in palatogenesis. However, the intracellular signaling pathway of TGF-β during palatogenesis in the anterior-posterior axis has not yet been fully understood. In the present study, the expression patterns of intracellular molecules Smad2/3 and phospho-p38 (Pp38) were examined at embryonic days 13.5, 14.0, and 14.5 (E13.5, E14.0, and E14.5) in mice. It was found that Smad3 was activated in anterior palatal mesenchyme and in the medial edge epithelium (MEE) region, with TGF-β3 expressed at E13.5. On the other hand, Pp38 was more expressed in posterior palatal mesenchyme and strongly expressed in the entire palatal epithelium at E13.5. These opposing expression patterns between Smad3 and Pp38 in palatal mesenchyme were also observed at E14.0. Interestingly, Pp38 expression was inhibited in MEE from E14.0. Generally, from E14.5, the tissue specificities of hard and soft palate started showing their characteristics following the activation of cell differentiation in palatal mesenchyme, and the medial edge seam (MES) of the palatal epithelium started to disappear for fusion to occur. At this stage, Smad3 was also more expressed in anterior palatal mesenchyme, while expression of Pp38 was activated in posterior palatal mesenchyme. Pp38 expression was inhibited, but Smad3 was activated in the MES. These results suggest that TGF-β signaling plays various roles, such as in cell proliferation and differentiation of palatal mesenchyme and in the disappearance of the MES, through different intracellular signaling pathways in anterior-posterior palatal mesenchyme and epithelium.

収録刊行物

• Journal of Hard Tissue Biology

  Journal of Hard Tissue Biology 25 (2), 195-204, 2016

  硬組織再生生物学会

キーワード

• TGF-β
• Smad
• p38
• Palate
• Development

詳細情報

• CRID: 1390282679435691136
• NII論文ID: 130005145107
• NII書誌ID: AA11074332
• DOI: 10.2485/jhtb.25.195
• ISSN: 1880828X
• ISSN: 13417649
• NDL書誌ID: 027250760
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I027250760
• Web Site: https://www.jstage.jst.go.jp/article/jhtb/25/2/25_195/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2016316639
• 本文言語コード: en
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可