| Project/Area Number |
13671218
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SHIGEMATSU Hiroshi The University of Tokyo, Faculty of Medicine, Associate Professor, 医学部附属病院, 助教授 (40134556)
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| Co-Investigator(Kenkyū-buntansha) |
KOYAMA Horoyuki The University of Tokyo, Faculty of Medicine, Associate Professor, 医学部附属病院, 助教授 (10241994)
大城 秀巳 東京大学, 医学部附属病院, 助手 (80272558)
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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 |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Balloon injury model / Intimal hyperplasia / TRAF6 / Inflammatory signaling pathway / Electroporation / In-stent restenosis / TRAF6 / 再障害モデル / ステント / ジーンチップ / 再障害 / バルーン障害 / 再狭窄 / ラビット |
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| Research Abstract |
We previously demonstrated that after stent implantation to rabbit carotid balloon injury model, replicating intimal cells were increased mainly in the inner intima, and abundant leukocytes adhered to the luminal surface. These findings suggest that inflammatory responses represent a unique property after stent implantation. TRAFG is an adaptor protain that mediate inflammatory signaling pathway, then we used plasmid-based electroporation method to transfer the dominant negative (DN) form of TRAFG to rabbit carotid artery. Inhibition of TRAF6 resulted in suppression of NFκB activity, BRK1/2 activity, cell proliferation, cell migration, and promotion of apoptosis that contributed to the prevention of neointimal formation after balloon injury. In the near future, we try to demonstrate the effect of TRAF6 on in-scent restenosis using stent implantation medel of rabbit carotid artery.
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