MiR-200b is involved in Tgf-beta signaling to regulate mammalian palate development
- Authors
- Shin, Jeong-Oh; Lee, Jong-Min; Cho, Kyoung-Won; Kwak, Sungwook; Kwon, Hyuk-Jae; Lee, Min-Jung; Cho, Sung-Won; Kim, Kye-Seong; Jung, Han-Sung
- Issue Date
- Jan-2012
- Publisher
- SPRINGER
- Keywords
- Palatogenesis; MiR-200b; Smad2; Snail; Apoptosis; Cell proliferation
- Citation
- HISTOCHEMISTRY AND CELL BIOLOGY, v.137, no.1, pp.67 - 78
- Indexed
- SCIE
SCOPUS
- Journal Title
- HISTOCHEMISTRY AND CELL BIOLOGY
- Volume
- 137
- Number
- 1
- Start Page
- 67
- End Page
- 78
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/166524
- DOI
- 10.1007/s00418-011-0876-1
- ISSN
- 0948-6143
- Abstract
- Various cellular and molecular events are involved in palatogenesis, including apoptosis, epithelialmesenchymal transition (EMT), cell proliferation, and cell migration. Smad2 and Snail, which are well-known key mediators of the transforming growth factor beta (Tgf-beta) pathway, play a crucial role in the regulation of palate development. Regulatory effects of microRNA 200b (miR-200b) on Smad2 and Snail in palatogenesis have not yet been elucidated. The aim of this study is to determine the relationship between palate development regulators miR-200b and Tgf-beta-mediated genes. Expression of miR-200b, E-cadherin, Smad2, and Snail was detected in the mesenchyme of the mouse palate, while miR-200b was expressed in the medial edge epithelium (MEE) and palatal mesenchyme. After the contact of palatal shelves, miR-200b was no longer expressed in the mesenchyme around the fusion region. The binding activity of miR-200b to both Smad2 and Snail was examined using a luciferase assay. MiR-200b directly targeted Smad2 and Snail at both cellular and molecular levels. The function of miR-200b was determined by overexpression via a lentiviral vector in the palatal shelves. Ectopic expression of miR-200b resulted in suppression of these Tgf-beta-mediated regulators and changes of apoptosis and cell proliferation in the palatal fusion region. These results suggest that miR-200b plays a crucial role in regulating the Smad2, Snail, and in apoptosis during palatogenesis by acting as a direct non-coding, influencing factor. Furthermore, the molecular interactions between miR-200b and Tgf-beta signaling are important for proper palatogenesis and especially for palate fusion. Elucidating the mechanism of palatogenesis may aid the design of effective gene-based therapies for the treatment of congenital cleft palate.
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