| Project/Area Number |
24790395
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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 |
Experimental pathology
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| Research Institution | Gunma University |
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Principal Investigator |
SETO Eri 群馬大学, 医学(系)研究科(研究院), 助教 (40431382)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Stress granule / P－body / 翻訳制御 / IL-6 / Macrophage / mRNP / ウイルス感染 |
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| Outline of Final Research Achievements |
Macrophages play fundamental roles in innate immunity. They consist of two main functional subsets, M1 and M2, which are differentially involved in inflammation and its resolution. In this study, the differences in the RNA metabolic machineries such as stress granules (SGs) and processing bodies (P-bodies) in M1- and M2-polarized human macrophage THP-1 cells were investigated. M1-THPs had less ability to assemble oxidative-stress-induced SGs than M2-THPs. In contrast, P-body assembly upon TLR4 stimulation was increased in M1-THPs as compared to M2-THPs. These results suggest that mRNA metabolism is controlled differently in M1-THPs and M2-THPs. Knocking down EDC4 or Dcp1a, which are components of P-bodies, severely reduced the production of IL-6 in M1-THPs without decreasing the amount of IL-6 mRNA, indicating that the formation of P-bodies containing EDC4 and Dcp1a is critical in the posttranscriptional regulation of IL-6.
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