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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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 一酸化窒素 / エンドサイトーシス / Rab5 / ファゴサイトーシス / 感染 / 歯周病 / タンパク質修飾 / ニトロシル化 / フリーラジカル / 炎症 / 酸化ストレス / 活性酸素 |
|---|
| 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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Report
(5 results)
Research Products
(25 results)
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[Journal Article] Periodontitis induced by bacterial infection exacerbates features of Alzheimer's disease in transgenic mice2017
Author(s)
Ishida N, Ishihara Y, Ishida K, Tada H, Funaki-Kato Y, Hagiwara M, Ferdous T, Abdullah M, Mitani A, Michikawa M, Matsushita K.
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Journal Title
NPJ Aging Mech. Dis.
Volume: 3
Issue: 1
Pages: 15-15
DOI
NAID
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Presentation] How is phagocytosis regulated by NO ?2014
Author(s)
Makoto Hagiwara, Ryutaro Isoda, Yoshiko Kato, Naoyuki Ishida, Jingshu Wang and Kenji Matsushita
Organizer
The 66the Annual Meeting of Japan Society for Cell biology
Place of Presentation
奈良
Year and Date
2014-06-11
Related Report
