The molecular mechanism for the generation of ROS through Nox
| Project/Area Number |
17K08637
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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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| Research Field |
General medical chemistry
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| Research Institution | Kawasaki Medical School (2018-2019)
Kyushu University (2017) |
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Principal Investigator |
Miyano Kei 川崎医科大学, 医学部, 助教 (60444783)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | Nox / 活性酸素 / 細胞遊走 / 上皮細胞 / 殺菌 / スーパーオキシド / NADPHオキシダーゼ / レドックス / 糖鎖修飾 / NADPH oxidase / ROS / membrane protein / redox |
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| Outline of Final Research Achievements |
Superoxide producing NADPH oxidase 1 (Nox1) that expresses abundantly in colon epithelium plays a crucial role in mucosal host defense. Previous studies have shown that Nox1 participates in epithelial migration which is an important process in mucosal wound healing. In this study, we investigated the effect of ROS scavenger’s pre-treatment on migration of human colon cancer HCT116 cells, which express Nox1. We found that Nox1 activity is positively feedbacked by its product itself, then the increased products depend on the regulation of migration ability of the cells.
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| Academic Significance and Societal Importance of the Research Achievements |
活性酸素は基本的に生体に有害であるため、Nox1の制御機構の破綻は、消化管上皮の疾患を引き起こす可能性がある。実際に、大腸がんの増悪とNox1の過剰な活性化の関連が指摘されており、どのようなメカニズムでNox1活性が調節を受けるのか、また、活性酸素がどのような分子メカニズムで遊走を制御しているのかを明らかにすることは重要な課題であった。今回の研究成果は、酸化ストレスにより引き起こされる様々な疾患の原因を明らかにする上で役立つものと考えられる。
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Report
(4 results)
Research Products
(5 results)
