| Project/Area Number |
09670194
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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 |
Human pathology
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| Research Institution | Miyazaki Medical College |
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Principal Investigator |
SUMIYOSHI Akinobu Miyazaki Medical College, 1st Department of Pathology, Professor, 医学部, 教授 (80038695)
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| Co-Investigator(Kenkyū-buntansha) |
KISANUKI Atsushi Miyazaki Medical College, 1st Department of Pathology, Research Assistant, 医学部, 助手 (70253846)
MARUTSUKA Kousuke Miyazaki Medical College, 1st Department of Pathology, Research Assistant, 医学部, 助手 (00239154)
ASADA Yujiro Miyazaki Medical College, 1st Department of Pathology, Associate Professor, 医学部, 助教授 (70202588)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | tissue factor / thrombus / atherosclerosis / smooth muscle cells / macrophages |
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| Research Abstract |
Thrombus formation on atherosclerotic plaques is the critical event in the development of acute coronary syndromes. We examined the localization, expression, and activity of tissue factor (TF), a primary initiator of the extrinsic coagulation pathway, in human and rabbit atherosclerotic lesions.
Immunohistochemically TF antigen was mainly observed in intimal smooth muscle cells (SMCs) and macrophages of human atherosclerotic lesions, and also in the extracellular matrix of the atheromatous plaques. A high level of TF activity was also detected in atherosclerotic lesions, particularly in advanced ones. In balloon-injured rabbit aortas, TF was rapidly induced in medial SMCs and was expressed in neointimal SMCs. Second balloon injury of the neointima without damage of neointimal SMCs induced platelet-rich thrombi on the injured surfaces. While the second injury with neointimal SMCs induced. fibrin-rich thrombi. The bolus injection of recombinant TF pathway inhibitor (rTFPI) markedly inhibited fibrin formation and neointimal growth following the second injury.
These results indicate that active TF is expressed in the : early stage of atherosclerotic lesions as well as in advanced lesions, and it contributes to the thrombotic property of atherosclerotic lesions. In addition, direct application of rTFPI to injured vessels may prevent thrombosis and restenosis following angioplasty.
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