| Project/Area Number |
14370742
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
ITOH Nobuyuki KYOTO UNIVERSITY Graduate school of Pharmaceutical Sciences, Professor, 薬学研究科, 教授 (10110610)
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| Co-Investigator(Kenkyū-buntansha) |
KONISHI Morichika KYOTO UNIVERSITY Graduate school of Pharmaceutical Sciences, Instructor, 薬学研究科, 助手 (00322165)
MIYAKE Ayumi KYOTO UNIVERSITY Graduate school of Pharmaceutical Sciences, Lecturer, 薬学研究科, 講師 (40346044)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥14,100,000 (Direct Cost: ¥14,100,000)
Fiscal Year 2003: ¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 2002: ¥7,200,000 (Direct Cost: ¥7,200,000)
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| Keywords | FGF / Adipose tissue / bone / Regeneration / Development / gene / Repair / 脂肪 / 軟骨 / 形成 |
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| Research Abstract |
The development of white adipose tissue (WAT) of Fgf10-/-mouse embryos was greatly impaired. We examined the mechanism of Fgf10 action in adipogenesis in vivo. The proliferative activity in the WAT of Fgf10-/-embryos was greatly decreased. Although the expression of C/EBP and PPAR in the WAT of Fgf10-/-embryos was greatly decreased, the expression of C/EBP was essentially unchanged. Although the expression of C/EBP and PPAR in the WAT was greatly decreased, the expression of Fgf10 was essentially unchanged. The present findings indicate that Fgf10 but not C/EBP is required for the proliferation of preadipocytes. In contrast, both Fgf10 and, C/EBP acting synergistically in separate, parallel pathways are required for the differentiation. Unexpectedly, the transcriptional cascade of adipogenesis in vivo described here is distinct from the cascade in vitro previously reported.
Fibroblast growth factor (FGF) signaling is also involved in skeletal development of the vertebrate. We show that Fgf18 is expressed in and required for osteogenesis and chondrogenesis in the mouse embryo. Fgf18 is expressed in both osteogenic mesenchymal cells and differentiating osteoblasts during calvarial bone development. In addition, Fgf18 is expressed in the perichondrium and joints of developing long bones. In calvarial bone, development of Fgf18-deficient mice generated by gene targeting, the progress of suture closure is delayed. Furthermore, proliferation of calvarial osteogenic mesenchymal cells is decreased, and terminal differentiation to calvarial osteoblasts is specifically delayed. Delay of osteogenic differentiation is also observed in the developing long bones of this mutant. Conversely, chondrocyte proliferation and the number of differentiated chondrocytes are increased. Therefore, FGF18 appears to regulate cell proliferation and differentiation positively in osteogenesis and negatively in chondrogenesis.
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