Elucidation of the regulatory mechanism of vascular morphology and development of methods to induce functional vascular structure
| Project/Area Number |
18K09782
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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 57060:Surgical dentistry-related
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| Research Institution | Hokkaido University |
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Principal Investigator |
Tamura Kiyomi 北海道大学, 歯学研究院, 助教 (90399973)
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 血管内皮細胞 / グリシン / PI3K / Akt / mTOR / SM22 / ゼブラフィッシュ / 血管発生 / 血管新生 / 転写調節 / 腫瘍 / 血管 |
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| Outline of Final Research Achievements |
Angiogenesis is a physiological phenomenon essential for individual development and the growth of tissues and organs. However, it is also involved in the occurrence and exacerbation of diseases such as tumors and chronic inflammatory diseases. Thus, elucidating the regulatory mechanisms of angiogenesis is an important task that not only improve our basic understanding, but also leads to the development of therapeutic treatments for diseases. In this study, we focused on vascular morphological change and revealed three regulatory mechanisms of angiogenesis: (1) the role of glycine in angiogenesis and the signaling pathway, (2) the interaction between PI3K-Akt-mTOR signaling and glycine in angiogenesis, and (3) a new role for the smooth muscle differentiation marker, SM22, in endothelial cells.
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| Academic Significance and Societal Importance of the Research Achievements |
低用量グリシンは血管新生を促進する一方、高用量は血管新生を抑制することを示した。この効果は、血管内皮細胞への直接作用の他、VEGFやNOによる間接作用を介して作用し、さらにPI3K-Akt-mTORシグナルとの相互作用を持つことが示された。グリシンの用量依存的な二相性効果は、血管構造の異常を起こさず血管長だけを変化させるため、機能的血管の制御において有用であると考えられる。
SM22が血管内皮細胞の伸長機能に伴い発現し、血管伸長を抑制する分子であることを明らかにした。SM22の発現は、病的血管において増加することが知られている。本研究によって、病的血管におけるSM22の役割が示唆された。
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Report
(6 results)
Research Products
(19 results)
