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研究発表を行った学会；
・第４０回日本発生生物学会・第５９回日本細胞生物学会　合同大会、2007年 5月28~30日(福岡)

タイトル；A possible role for FGF7-FGFR2 signaling in pancreatic development of the chick embryo.
発表者；　勝　賢二郎　氏
　　　（熊本大学　発生医学研究センター　パターン形成分野）
Abstract；
The primordia of the internal organ develop from foregut endoderm through interaction between epithelial and mesenchymal tissues. Several studies in mammals have demonstrated that mesenchymal signals control proliferation, differentiation and morphogenesis of pancreatic epithelium and that FGF and EGF family are involved in the mesenchymal signals. Fgf10 appears to have important roles in pancreatic development since mice lacking Fgf10 function show severe defects in growth and morphogenesis of pancreatic epithelium due to a dramatic reduction in the proliferation of the pancreatic progenitor cells.
In this study, we demonstrated that Fgf7 is strongly expressed in pancreatic mesenchyme of developing chick embryo. Fgf7 is detectable in splanchnic mesoderm surrounding pancreatic epithelium from Hamburger-Hamilton stage 18 (HH18). In contrast, Fgf10 is expressed at very low level in pancreatic mesenchyme. Fgf receptor 2 (Fgfr2) is strongly expressed in pancreatic epithelium, suggesting that FGF7-FGFR2 signaling has essential roles in pancreas formation in the chick embryo. To test this hypothesis, we introduced retroviral vectors carrying Fgf7 or mutated Fgfr2 into presumptive pancreatic endoderm at HH 12 by in ovo electroporation and assessed the formation of dorsal pancreatic bud at HH 21-22 by analyzing the expression of pancreatic marker genes. Overexpression of a dominant-negative Fgfr2 gene, which lacked intracellular tyrosine kinase domain, resulted in reduced outgrowth of the pancreatic bud. In addition, our preliminary findings suggest that activation of FGF signaling by overexpression of Fgf7 or constitutively active Fgfr2 promote outgrowth of the pancreatic bud. These results suggest that, in chick embryos, FGF7-FGFR2 signaling might play an important role in the outgrowth of pancreatic bud probably by promoting proliferation of the pancreatic precursor.