Establishment of evaluation method for arteriosclerotic lesions by measuring the "hardness" of blood vessels using an atomic force microscope
| Project/Area Number |
18K08729
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 55030:Cardiovascular surgery-related
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| Research Institution | Mie University |
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Principal Investigator |
matsuo eri 三重大学, 医学部附属病院, 技術補佐員 (40751665)
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| Co-Investigator(Kenkyū-buntansha) |
島本 亮 三重大学, 医学部附属病院, 准教授 (90324524)
岡本 貴行 島根大学, 学術研究院医学・看護学系, 准教授 (30378286)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 動脈硬化 / 血管内皮 / YAP/TAZ / 血管内皮細胞 / 血管新生 / 基質の硬さ |
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| Outline of Final Research Achievements |
Arteriosclerosis plaques have tissue changes such as fatty, fibrotic, and calcified as the disease progresses. In this study, we elucidate how vascular endothelial cells regulate the sensitivity of extracellular matrix to hardness and regulate cell function in arteriosclerotic plaques. We cultured vascular endothelial cells on extracellular matrix with different hardness, and examined how the hardness of the substrate controls cell function. Soft substrates inactivate YAP, induce Dll4, activate Notch signals, induce angiogenesis-related receptors, the coagulation factors thrombomodulin, TF, and suppress the expression of the anti-inflammatory cytokine IL-6. It was shown that the hardness of blood vessels contributes to the regulation of the function of vascular endothelial cells.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の目的は、動脈硬化病変における基質の硬さに対する血管内皮細胞機能の制御機構の解明である。動脈硬化症のプラークは、病状の進行により脂肪性から、線維化、石灰化まで組織が変化し硬化していく。本研究では、血管の硬さが血管内皮細胞の機能を調節する一因となることを示した。プラークにおいて、内皮細胞が力学的変化を感知する分子機構の解明することにより、プラーク組織の力学的性質を評価し、抗血栓性および抗炎症性などの内皮細胞機能を制御することができれば、心臓血管領域の発展に繋がる。
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Report
(4 results)
Research Products
(2 results)
