TY - JOUR
T1 - Sprouty2 controls proliferation of palate mesenchymal cells via fibroblast growth factor signaling
AU - Matsumura, Kaori
AU - Taketomi, Takaharu
AU - Yoshizaki, Keigo
AU - Arai, Shinsaku
AU - Sanui, Terukazu
AU - Yoshiga, Daigo
AU - Yoshimura, Akihiko
AU - Nakamura, Seiji
N1 - Funding Information:
This work was supported by special grants-in-aid from the Ministry of Education, Culture, Sports, Science and Technology of Japan .
Copyright:
Copyright 2011 Elsevier B.V., All rights reserved.
PY - 2011/1/28
Y1 - 2011/1/28
N2 - 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.
AB - 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.
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U2 - 10.1016/j.bbrc.2010.12.116
DO - 10.1016/j.bbrc.2010.12.116
M3 - Article
C2 - 21195053
AN - SCOPUS:79151470752
VL - 404
SP - 1076
EP - 1082
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 4
ER -