| Project/Area Number |
09281104
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas (A)
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| Allocation Type | Single-year Grants |
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
KITA Toru Kyoto University Professor, 医学研究科, 教授 (60161460)
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| Co-Investigator(Kenkyū-buntansha) |
MUROTA Sei-itsu Tokyo Medical and Dental University Professor, 医歯学総合研究科, 教授 (50072989)
SATOH Yasufumi Tohoku University Professor, 医学研究科, 教授 (50178779)
NAGAI Ryozo Tokyo University Professor, 医学系研究科, 教授 (60207975)
KODAMA Tatsuhiko Tokyo University Professor, 先端科学技術センター, 教授 (90170266)
SHIBUYA Masabumi Tokyo University Professor, 医学系研究科, 教授 (10107427)
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| Project Period (FY) |
1997 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥259,200,000 (Direct Cost: ¥259,200,000)
Fiscal Year 2001: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2000: ¥44,100,000 (Direct Cost: ¥44,100,000)
Fiscal Year 1999: ¥61,500,000 (Direct Cost: ¥61,500,000)
Fiscal Year 1998: ¥66,900,000 (Direct Cost: ¥66,900,000)
Fiscal Year 1997: ¥83,700,000 (Direct Cost: ¥83,700,000)
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| Keywords | Atherosclerosis / Vascular endothelial cell / Vasculogenesis / Angiogenesis / Vascular smooth muscle cell / Phenotypic conversion / Adhesion molecule / Oxidized LDL / 脈管形成 / ずり応力 / 遺伝子導入 |
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| Research Abstract |
The Grants-in-Aid for Scientific Research on Priority Areas No. 09281104 was issued from 1997 to 2000. During the period, we organized a research group with scientists who are considered to be most active in the research field. Atherosclerosis is correlated with a variety of vascular disorders such as coronary heart disease. We therefore placed our goal on elucidation of the molecular mechanism of atherosclerosis and exploration of novel therapeutic strategies. To conduct investigation, the members were divided into 3 subgroups, i.e. Group 1, 2, and 3 with different subject of study as follows. We also formed a Central Committee to coordinate and facilitate the research activity of the subgroups.
[Group 1] Study subject : Molecular mechanism of vascular formation. Atherosclerosis has been considered to evolve according to the mechanism shared with vascular formation in the body. During the research period, we have made a significant progress in understanding vasculogenesis and angiogene
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sis. In Conclusion, the roles of new molecules such as transcription factor ets-1 and other molecules were clarified. [Group 2] Study subject : Endothelial dysfunction and blood cells. There has been accumulating evidence that atherosclerosis is initiated by endothelial dysfunction due to a variety of biological insults. We therefore formed this subgroup to explore the key molecules involved in those events. We discovered novel scavenger receptors such as LOX-1 and SRPSOX. Furthermore, we revealed that adipose tissues produce cytokines abundantly. Among those cytokines, adiponectin has been shown to play an important role in atherogenesis and insulin resistance. [Group 3] Study subject : Molecular mechanism of phenotypical conversion and proliferation of vascular smooth muscle cells. This subgroup focused on the mechanism of phenotypical conversion of vascular smooth muscle cells, which is believed to be the characteristic feature of the advanced atherosclerotic lesions. To clarify these points, a variety of transcription factors such as BTBE2 were examined. Also, the new methods to deliver genes were developed.
In conclusion, we have made a successful progress in atherosclerosis research, which will be translated into clinical application in the near future. Less
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