| Project/Area Number |
18H03375
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 63020:Radiation influence-related
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
松井 理 金沢医科大学, 医学部, 助教 (60288272)
逆井 良 金沢医科大学, 医学部, 講師 (10549950)
砂谷 優実 金沢医科大学, 医学部, 講師 (70581057)
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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 |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2020: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥8,320,000 (Direct Cost: ¥6,400,000、Indirect Cost: ¥1,920,000)
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| Keywords | アポトーシス / DNA損傷 / 53BP1 |
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| Outline of Final Research Achievements |
Apoptotic cells express chromatin on the surface of cell membrane. Macrophages quickly removes apoptotic cells by phagocytosis. When this removal of apoptotic cells is inefficient, the histone and DNA on the surface of apoptotic cells are believed to become an auto-antigen to trigger auto-antibody production, which then leads to autoimmune diseases, such as systemic lupus erythematosus. We found that deficiency of DNA repair protein 53BP1 slightly reduced the expression of chromatin on the cell surface of apoptotic cells.
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| Academic Significance and Societal Importance of the Research Achievements |
アポトーシス細胞の表層にはクロマチンが露出する。体内に発生したアポトーシス細胞はマクロファージにより速やかに貪食され除去されるが、この貪食の進行に障害が起こると、細胞表層のクロマチンが自己抗体産生の自己抗原になるとされている。本研究の成果は、SLEを代表とする自己免疫疾患の発症メカニズムに大きな知見を与える可能性がある。
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