| Project/Area Number |
15K15196
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Laboratory medicine
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| Research Institution | Kagoshima University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
丸山 征郎 鹿児島大学, 医歯学総合研究科, 特任教授 (20082282)
伊藤 隆史 鹿児島大学, 医歯学総合研究科, 講師 (20381171)
大山 陽子 鹿児島大学, 附属病院, 特任助教 (20583470)
竹之内 和則 鹿児島大学, 附属病院, 医員 (30646758)
清水 利昭 鹿児島大学, 医歯学域医学系, 助教 (50468055)
橋口 照人 鹿児島大学, 医歯学域医学系, 教授 (70250917)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | microRNA / 血管内皮細胞 / 単核球 / 単球 / miRNA / エクソゾーム / 一酸化窒素 |
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| Outline of Final Research Achievements |
The evaluation of vascular endothelial function is mainly based on physiological function tests, such as ABI and FMD, which measure vasodilatation action. Since nitric oxide (NO) regulates the elasticity of blood vessels, we examined miRNAs that cause alteration of the level of NO. Vascular endothelial cells, HUVEC and HAEC, increase NO production by insulin and cytokines. Bacterial infection upregulates miR-218 level in monocytic cells. This increase of miR-218 suppresses the level of inflammatory cytokines in monocytic cells, suggesting that monocytic miRNA can indirectly regulate NO production in endothelial cells. We have shown the communication between monocytic cells to endothelial cells control vascular function mediated by mRNAs.
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