AI Article Synopsis
- TGF-beta 3 plays a key role in regulating the disappearance of medial edge epithelium (MEE) during the process of palatal fusion in mice.
- SMAD2, a mediator of TGF-beta signaling, is primarily expressed in the MEE and its phosphorylation is essential for normal development and fusion, as shown by the effects of Smad2 siRNA transfection which inhibited its expression.
- The study found that reducing SMAD2 levels led to persistent MEE cells and increased cell proliferation, indicating that endogenous SMAD2 is critical for MEE disappearance during palatal fusion.
Article Abstract
Transforming growth factor (TGF)-beta 3 is known to regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Our previous studies showed that SMAD2, a TGF-beta signaling mediator, was expressed and phosphorylated primarily in the MEE and that SMAD2 phosphorylation in the MEE was temporospatially regulated by TGF-beta 3. The goal of this study was to examine the requirement for SMAD2 to complete the developmental events necessary for palatal fusion. SMAD2 expression was inhibited with Smad2 siRNA transfection into palatal tissues in vitro. The results showed that Smad2 siRNA transfection resulted in the maintenance of MEE cells in the palatal midline. Western blot and immunofluorescence analyses confirmed that the endogenous SMAD2 and phospho-SMAD2 levels were reduced following siRNA transfection. The SMAD3 level was not altered by the Smad2 siRNA transfection. The persistence of the MEE and the decreased SMAD2/phospho-SMAD2 levels were coincident with increased MEE cell proliferation. Addition of exogenous TGF-beta 3 increased p-SMAD2 level but not the total SMAD2 level. Therefore, exogenous TGF-beta 3 was not able to induce p-SMAD2 enough to rescue the palatal phenotype in the Smad2 siRNA group. The results indicated that the endogenous SMAD2 level is crucial in the regulation of disappearance of MEE during palatal fusion.
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| http://dx.doi.org/10.1002/dvdy.20819 | DOI Listing |
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