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Updated: Jun 5, 2026

Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes
Published on: February 13, 2021
Sprouty2 controls proliferation of palate mesenchymal cells via fibroblast growth factor signaling
Kaori Matsumura1, Takaharu Taketomi, Keigo Yoshizaki
1Section of Oral and Maxillofacial Oncology, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Abstract:
Cleft palate is one of the most common craniofacial deformities. The fibroblast growth factor (FGF) plays a central role in reciprocal interactions between adjacent tissues during palatal development, and the FGF signaling pathway has been shown to be inhibited by members of the Sprouty protein family. In this study, we report the incidence of cleft palate, possibly caused by failure of palatal shelf elevation, in Sprouty2-deficient (KO) mice. Sprouty2-deficient palates fused completely in palatal organ culture. However, palate mesenchymal cell proliferation estimated by Ki-67 staining was increased in Sprouty2 KO mice compared with WT mice. Sprouty2-null palates expressed higher levels of FGF target genes, such as Msx1, Etv5, and Ptx1 than WT controls. Furthermore, proliferation and the extracellular signal-regulated kinase (Erk) activation in response to FGF was enhanced in palate mesenchymal cells transfected with Sprouty2 small interfering RNA. These results suggest that Sprouty2 regulates palate mesenchymal cell proliferation via FGF signaling and is involved in palatal shelf elevation.
Insights
Sprouty2 deficiency in mice leads to increased palate cell proliferation and potential cleft palate. This suggests Sprouty2 regulates palatal shelf elevation through fibroblast growth factor (FGF) signaling.
Area of Science:
- Developmental biology
- Genetics
- Craniofacial research
Background:
- Cleft palate is a common craniofacial deformity.
- Fibroblast growth factor (FGF) signaling is crucial for palatal development.
- Sprouty proteins inhibit FGF signaling pathways.
Purpose of the Study:
- Investigate the role of Sprouty2 in palatal development.
- Determine the incidence of cleft palate in Sprouty2-deficient mice.
- Elucidate the mechanism by which Sprouty2 affects palatal shelf elevation.
Main Methods:
- Sprouty2-deficient (KO) and wild-type (WT) mice were used.
- Palatal organ culture was performed to assess fusion.
- Cell proliferation was measured using Ki-67 staining.
- Gene expression of FGF target genes (Msx1, Etv5, Ptx1) was analyzed.
- In vitro experiments used small interfering RNA (siRNA) to inhibit Sprouty2.
Main Results:
- Sprouty2-deficient palates showed complete fusion in organ culture.
- Palate mesenchymal cell proliferation was significantly increased in Sprouty2 KO mice.
- Sprouty2-null palates exhibited higher expression of FGF target genes.
- Inhibition of Sprouty2 enhanced FGF-induced proliferation and Erk activation in mesenchymal cells.
Conclusions:
- Sprouty2 plays a critical role in regulating palate mesenchymal cell proliferation.
- Sprouty2 acts via the FGF signaling pathway.
- Sprouty2 is involved in the process of palatal shelf elevation, and its deficiency may lead to cleft palate.
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