| Project/Area Number |
10557090
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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 |
Hematology
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| Research Institution | Nagoya University |
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Principal Investigator |
KOJIMA Tetsuhito Nagoya University, School of Medicine, Associate Professor, 医学部, 助教授 (40161913)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Koji School of Medicine, Medical Staff, 医学部, 医員
KADOMATSU Kenji School of Medicine, Associate Professor, 医学部, 助教授 (80204519)
都築 忍 名古屋大学, 医学部, 医員
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥13,200,000 (Direct Cost: ¥13,200,000)
Fiscal Year 1999: ¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1998: ¥6,800,000 (Direct Cost: ¥6,800,000)
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| Keywords | Heparan sulfate proteoglycan / ryudocan (syndecan-4) / null mice / focal adhesion / fibronectin / Ryudocan / ノックアウトマウス / 血中濃度 / 心筋梗塞 / 組織修復 |
|---|
| Research Abstract |
Focal adhesion formation on fibronectin requires two signals, i.e. one from the cell-binding domain of fibronectin and one from the heparin-binding domain. While the cell-binding domain is recognized by integrins, the cell surface molecules that recognize the heparin-binding domain have not been identified. Previous reports have demonstrated that ryudocan (syndecan-4), a heparan sulfate proteoglycan, is a component of focal adhesions and that anti-syndecan-4 antibody can promote focal adhesion formation. Thus, ryudocan is a candidate that recognizes the heparin-binding domain. To study the role of syndecan-4 in focal adhesion formation, we generated ryudocan null mice. Even in ryudocan (-/-) fibroblasts, focal adhesions were formed and actin fibers terminated normally at focal adhesions. However, neither the fibronectin heparin-binding fragment in a soluble form nor anti-ryudocan antibody promoted focal adhesion formation in ryudocan (-/-) fibroblasts cultured on the cell-binding fragment, promoted focal adhesion formation. Thus, the present study has revealed that the heparin-binding fragment in a soluble form requires ryudocan for focal adhesion formation, whereas one in a solid form could utilize not only ryudocan but also some unidentified cell surface molecules.
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