Sprouty2 controls proliferation of palate mesenchymal cells via fibroblast growth factor signaling

Kaori Matsumura, Takaharu Taketomi, Keigo Yoshizaki, Shinsaku Arai, Terukazu Sanui, Daigo Yoshiga, Akihiko Yoshimura, Seiji Nakamura

Research output: Contribution to journalArticlepeer-review

39 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1076-1082
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number4
Publication statusPublished - 2011 Jan 28


  • Cell proliferation
  • Cleft palate
  • FGF signaling
  • Sprouty2-deficient mice

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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