Title: Smad2 Overexpression Rescue the Secondary Palate Cleft by Increasing Apoptosis
Husein Al-Omer (Presenter)
Prince Abdul Rahman Advanced Dental Institue, Prince Sultan Military Medical City, Medical Services, Ministry of Defence and Aviation
Gihan Gawish, College of Medicine, Al Imam Muhammad Ibn Saud Islamic University
Objectives: Mammalian palatogenesis is a highly regulated morphogenetic process during which the embryonic primary and secondary palatal shelves develop as outgrowths from the medial nasal and maxillary prominences, respectively, remodel and fuse to form the intact roof of the oral cavity. The aim of this study was to understand the mechanism of palatal fusion in the rescuesecondary palate cleft compared to wild-type.
Methods: Smad2 overexpression and wild-type genetic models were used. Serial 7 micron sections were studied for detection of apoptosis and epithelial mesenchymal transition. Then, activation of Smad2 was studied with phospho-Smad2 antibody, and the level of Smad2 in each embryonormalized with immuneflorescence.
Results: We observed that the effect of the K14-Smad2 expression was analyzed in the medial edge epithelium of the rescue mice; the MEE had a much higher ratio of cells with cleaved caspase, a marker of apoptosis, than in the control fused palates. The increase in apoptosis was correlated with increased p-Smad2 in the same cells, while p- Smad2 in the control mice with normal palatal fusion was not associated with high levels of apoptotic MEE.
Conclusions: We concluded that Smad2 overexpression might rescue the cleft in the secondary palate by increasing apoptosis of epithelial cells in the middle seam