Mechanism of progression of neointimal hyperplasia at the vasada anastomatic strictwe : a study in tenascin-C Deficient Mice
| Project/Area Number |
14370409
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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 |
Thoracic surgery
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| Research Institution | Mie University |
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Principal Investigator |
ONODA Koji Mie University, University Hospital, Assistant professor, 医学部附属病院, 講師 (70260601)
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| Co-Investigator(Kenkyū-buntansha) |
IMANAKA Kyoko (YOSHIDA Kyoko) Mie University, Faculty of Medicine, Assistant Professor, 医学部, 講師 (00242967)
YOSHIDA Toshiuchi Mie University, Faculty of Medicine, Professor, 医学部, 教授 (80166959)
YADA Isao Mie University, Faculty of Medicine, Professor, 医学部, 教授 (80093152)
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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 |
¥5,900,000 (Direct Cost: ¥5,900,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥4,400,000 (Direct Cost: ¥4,400,000)
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| Keywords | Tenascin-C / Vasculai grafto stricture / extracellular matrix / intimal hyperplasia / antery graft stenosis / immuno histochemistry / Knock-out mouse |
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| Research Abstract |
A simple aortotomy model was constructed using mice. In the wild-type mice, neointimal hyperplasia was observed at the suture sites at days 14 and 28. Immunohistochemical staining showed the strong expression of tenascin-C in both the neoinitima and media around the suture line at day 14. At day 28, tenascin-C staining was detected in the neointima, but not in the media. In the tenascin-C-deficient mice, much less neointimal hyperplasia was seen compared to in the wild-type mice and the mean neointima/media area ratio decreased to 45.4% and 30.5% at days 14 and 28, respectively. Proliferating cell nuclear antigen indeces in the wild-type mice were two times higher than those in the tenascin-C-deficient mice at day 14. Less alcian blue-positive proteoglycans were deposited in the neointima of the tenascin-C-deficient mice than the wild-type mice. These results suggest that tenascin-C promotes neointimal cell migration and proliferation, and deposition of proteoglycans. The current study provide direct evidence that tenascin-C is a key molecule in neointimal hyperplasia in anastomotic stenosis, implying its role as a target molecule for the prevention of stenosis.
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Report
(3 results)
Research Products
(5 results)
