| Project/Area Number |
13670725
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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 |
Circulatory organs internal medicine
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| Research Institution | Nagasaki University |
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Principal Investigator |
KAWANO Hiroaki University Hospital, Assistant, 医学部附属病院, 助手 (30325659)
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| Co-Investigator(Kenkyū-buntansha) |
YANO Katsusuke Course of Medical and Dental Science, Graduate School of Biomedical Science, Professor, 大学院・医歯薬総合研究科, 教授 (50039864)
SETO Shinji Course of Medical and Dental Science, Graduate School of Biomedical Science, Associate professor, 大学院・医歯薬総合研究科, 助教授 (00136657)
ASHIZAWA Naoto University Hospital, Lecturer, 医学部附属病院, 講師 (10301368)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | integrin / cardiac remodeling / hypertension / fibroblast / extracellular matrix / cardiac function / 心エコー |
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| Research Abstract |
Integrins are a family of transmembrane receptors which were mainly studied on angiogenesis and metastasis of malignant tumor. The interaction of integrins with extracellular matrix protein promotes cell adhesion, spreading, cell migration, and cell proliferation, and they seem to be related to cardiovascular disease. Recently, the beta 1 integrin has been implicated in cardiac hypertrophy. We have researched about the effect of interstitium on cardiac function, especially cardiac fibroblast and integrin system. Integrin system is complicated because more than twenty types of integrins and many types of extracellular matrix proteins. We have already reported that angiotensin II enhances αV, β3, and β5 integrin expressions in cardiac fibroblast and adhesion of cardiac fibroblast to extracellular matrix proteins. Moreover, αV, β3, and β5 integrins of vascular smooth muscle cells, and they are related to vascular smooth muscle cell migration which is related to atherosclerosis.
In 2K1C hypertensive heart, these integrins were increased, focal adhesion kinase was activated, and they were accompanied with cardiac remodeling and diastolic dysfunction.
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