| Project/Area Number |
13557202
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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 | 展開研究 |
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| Research Field |
Biological pharmacy
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
ITOH Nobuyuki ITOH,Nobuyuki, 薬学研究科, 教授 (10110610)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMOTO Masatumi Shionogi Co., Research Laboratories, Senior Scientist, 創薬第二研究所, 主席研究員
OHTA Mitsuhiro Kobe Pharmaceutical University, Professor, 教授 (00330423)
KONISHI Morichika KYOTO UNIVERSITY, Graduate School of Pharmaceutical Science, Instructor, 薬学研究科, 助手 (00322165)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥13,700,000 (Direct Cost: ¥13,700,000)
Fiscal Year 2003: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2002: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2001: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Keywords | FGF / Adipose tissue / bone / Regeneration / Development / gene / Repair / Against / 組組修復 |
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| Research Abstract |
Fgf18 is expressed in both osteogenic mesenchymal cells and differentiating osteoblasts during calvarial bone development. In calvarial bone development bf 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. Conversely, chondrocyte proliferation and the number of difrerentiated chondrocytes are increased. Therefore, FGF18 appears to regulate cell proliferation and iffelentiation posltively in osteogenesis and negatively in chondrogenesis.
The development of white adipose tissue(WAT) off Fgf10-1-mouse embryos was greatly impaired. We examined the mechanism of Fgf10 action in adipogenesis in vivo. The proliferative activity in the WAT of Fgf10-1-embryos was greatly decreased, Although the expression of ClEBP and PPAR in the WAT of Fgf10-1-embryos was greatly dereased, the expression of CIEBP was essentially unchanged. Although the expression of CIEBP and PPAR in the WAT was greatly decreased, the expression of Fgf10 was essentially unchanged. The present findings indicate that Fgf10 but not ClEBP is required for the proliferation of preadipocytes. In coontrast,both Fgf10 and CIEBP acting synergistically in separate, parallel pathways are required for the differentiation. Unexpectedly, thetranscriptional cascade of adipogenesis in vivo described here is distinct from the cascade in vivo previously reported.
We also examined Fgf-like molecules of low molecular weighs by random pepptide library using recombinant Fgf receptors. We identified some candidate molecules. We examined the activity of these molecules using cultured cells that expressed Fgf receptors.These molecules were found to have weak but significan tFgf-like activity.
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