2003 Fiscal Year Final Research Report Summary
The pathophysiological study of mechanisms which contribute to in-stent restenosis
| 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)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Balloon injury model / Intimal hyperplasia / TRAF6 / Inflammatory signaling pathway / Electroporation / In-stent restenosis |
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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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