2017 Fiscal Year Final Research Report
Oral tissue inflammation cellular generate gases that cause cellular function failure.
| Project/Area Number |
26861586
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | University of Niigata Prefecture (2015-2017)
National Center for Geriatrics and Gerontology (2014) |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | 一酸化窒素 / エンドサイトーシス / Rab5 |
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| Outline of Final Research Achievements |
Nitric oxide (NO), produced from L-arginine by nitric oxide synthases (NOSs) in cells, modulates post-translational proteins. Recent studies have been reported covalent adduction of a NO moiety to cysteines called S-nitrosylation is a key NO signaling pathway and regulates protein functions. Here, we report that NO regulates phagocytosis through S-nitrosylation of Rab5. To investigate the effect of NO on phagocytosis, we treated RAW264 cells with a NO donor GSNO. Phagocytosis was facilitated in RAW264 cells by treatment with GSNO. We next examined the effect of NO on Rab5 activity. As a result of GST-R5BD pull down assay, Rab5 activity was augmented by treatment with NO in cultured cells. We evaluated S-nitrosylation of Rab5 by using biotin switch methods. S-nitrosylation was observed in active Rab5 more strongly than inactive Rab5. Collectively, our date suggests a mechanism by which NO activates Rab5 and phagocytosis through S-nitrosylation.
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| Free Research Field |
歯学
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