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TGF-β Signaling and the Epithelial-Mesenchymal Transition during Palatal Fusion
Akira Nakajima1, Charles F Shuler2, Alexander O D Gulka3
1Department of Orthodontics, Nihon University School of Dentistry, Chiyoda-ku, Tokyo 101-8310, Japan. nakajima.akira@nihon-u.ac.jp.
International Journal of Molecular Sciences
|November 23, 2018
Summary
Transforming growth factor-beta (TGF-β) signaling is crucial for palate fusion, guiding medial edge epithelial (MEE) cell fate. This study clarifies TGF-β
Area of Science:
- Developmental Biology
- Molecular Signaling
- Craniofacial Development
Background:
- Palatogenesis involves palate fusion, separating nasal and oral cavities.
- Medial edge epithelial (MEE) cells are critical for palatal fusion.
- MEE cells are lost from the midline seam via migration, EMT, or apoptosis.
Purpose of the Study:
- To define the role of transforming growth factor-beta (TGF-β) signaling in MEE cell fate during palatal fusion.
- To summarize current understanding of TGF-β signaling in palatogenesis.
Main Methods:
- Organ culture with small interfering RNA (siRNA) targeting TGF-β receptors.
- Genetically engineered mice (e.g., Wnt1-cre/R26R double transgenic).
- Cell lineage tracing using cell fate markers.
Main Results:
- TGF-β3 and Smad2 are preferentially expressed in critical fusion cells.
- TGF-β type 3 receptor is essential for palatal fusion, confirmed by Cre-lox and siRNA.
- TGF-β signaling critically regulates MEE cell fate during palate fusion.
Conclusions:
- TGF-β signaling, particularly TGF-β3, is vital for regulating MEE cell behavior during palatal fusion.
- The accessory receptor TGF-β type 3 receptor plays a critical role, indicating high ligand demand.
- Further insights into MEE cell fate within the midline epithelial seam (MES) are provided, focusing on TGF-β's role.
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