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MiR-200b is involved in Tgf-β signaling to regulate mammalian palate development.

 Jeong-Oh Shin  ;  Jong-Min Lee  ;  Kyoung-Won Cho  ;  Sungwook Kwak  ;  Hyuk-Jae Kwon  ;  Min-Jung Lee  ;  Sung-Won Cho  ;  Kye-Seong Kim  ;  Han-Sung Jung 
 HISTOCHEMISTRY AND CELL BIOLOGY, Vol.137(1) : 67-78, 2012 
Journal Title
Issue Date
Animals ; Apoptosis ; Cadherins/genetics ; Cadherins/metabolism ; Cell Proliferation ; HEK293 Cells ; Humans ; Immunohistochemistry ; Mice ; Mice, Inbred ICR ; MicroRNAs/genetics ; MicroRNAs/metabolism* ; Palate/cytology ; Palate/growth & development* ; Palate/metabolism* ; Real-Time Polymerase Chain Reaction ; Signal Transduction*/genetics ; Smad2 Protein/genetics ; Smad2 Protein/metabolism ; Snail Family Transcription Factors ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism*
Palatogenesis ; MiR-200b ; Smad2 ; Snail ; Apoptosis ; Cell proliferation
Various cellular and molecular events are involved in palatogenesis, including apoptosis, epithelial-mesenchymal transition (EMT), cell proliferation, and cell migration. Smad2 and Snail, which are well-known key mediators of the transforming growth factor beta (Tgf-β) 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-β-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-β-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-β 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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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Others (기타) > 1. Journal Papers
Yonsei Authors
Kwon, Hyuk Jae(권혁제)
Shin, Jeong Oh(신정오) ORCID logo https://orcid.org/0000-0002-6935-0936
Lee, Min Jung(이민정)
Lee, Jong Min(이종민) ORCID logo https://orcid.org/0000-0002-9466-7644
Jung, Han Sung(정한성) ORCID logo https://orcid.org/0000-0003-2795-531X
Cho, Kyoung Won(조경원)
Cho, Sung Won(조성원) ORCID logo https://orcid.org/0000-0001-7505-9769
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