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RNA sequencing of mouse palatal epithelial cells following TGF-β3 treatment or Tgfb3 knockdown

ABSTRACT: Epithelial-mesenchymal transition (EMT) of medial edge epithelial cells is a critical mechanism underlying embryonic palatal fusion, driven by transforming growth factor beta 3 (TGF-β3). However, its regulatory interplay with downstream cascades remains poorly understood. To elucidate cellular reprogramming mechanisms during palatogenesis, embryonic day 15 C57BL6/J mouse palatal epithelial cells were isolated to eliminate mesenchymal interference. To evaluate transcriptomic shifts, next-generation RNA sequencing was performed on cells cultured in three groups: a control group (no treatment), a group treated with 1 ng/mL of recombinant TGF-β3 to induce EMT, and a group with siRNA transfection Tgfb3 knockdown. This dataset provides the global gene expression profiles underlying TGF-β3-mediated palatal fusion, revealing EMT as the main pathway.

ORGANISM(S): Mus musculus

PROVIDER: GSE343560 | GEO | 2026/09/11

REPOSITORIES: GEO

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Project description:Cleft palate results from a mixture of genetic and environmental factors and occurs when the bilateral palatal shelves fail to fuse. The objective of this study was to search for new genes involved in mouse palate formation. Gene expression of murine embryonic palatal tissue was analyzed at the various developmental stages before, during, and after palate fusion using GeneChip? microarrays. Ceacam1 was one of the highly up-regulated genes during and after fusion in palate formation, and this was confirmed by quantitative real-time PCR. Immunohistochemical staining showed that CEACAM1 was expressed at a very low level in palatal epithelium before fusion, but highly expressed in the midline of the palate during and after fusion. To investigate the developmental role of CEACAM1, function-blocking antibody was added to embryonic mouse palate in organ culture. Palatal fusion was inhibited by this function-blocking antibody. To investigate the subsequent developmental role of CEACAM1, we characterized Ceacam1-deficient (Ceacam1-/-) mice. Epithelial cells persisted abnormally at the midline of the embryonic palate even on day E16.0, and palatal fusion was delayed in Ceacam1-/- mice. TGF?3 expression, apoptosis, and cell proliferation in palatal epithelium were not effected in the palate of Ceacam1-/-mice. CEACAM1 expression was down-regulated in Tgfb3-/- palate. However, exogenous TGF?3 did not induce CEACAM1 expression. These results suggest that CEACAM1 has roles in both the initiation of palate formation via epithelial cell adhesion and TGF signaling has some indirect effect on CEACAM1. Global gene expression profiling of palatal processes before, during and after fusion of palatal shelves We used microarray to investigate the gene expression of palatal tissue during palatal development. Palatal processes were microdissected at the stages of palatal development (before, during and after fusion) for RNA extraction and hybridization on Affymetrix microarrays.

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RNA sequencing of mouse palatal epithelial cells following TGF-β3 treatment or Tgfb3 knockdown

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