| Project/Area Number |
16K09896
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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 |
Collagenous pathology/Allergology
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| Research Institution | Okayama University |
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Principal Investigator |
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| Research Collaborator |
ASANO Sumie (Hiramatsu Sumie)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | SLE / S1PR1 / miR223 / T細胞 / apoptosis / T cell / epigenetics / 免疫学 |
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| Outline of Final Research Achievements |
The reduction of sphingosine 1 phosphate receptor 1 (S1PR1) expression in systemic lupus erythematosus (SLE) is reported. We confirmed the upregulation of microRNA223-3p (miR223), which suppresses the expression of S1PR1, in the splenic T cells in MRL/lpr lupus-prone mice. We constructed and analyzed miR223 knockout B6/MRL mice. The proportion of early apoptosis cells in peripheral lymphatic CD4+ T cells was significantly increased, and the numbers of CD19+ cells, CD19+CD138+ cells and CD138+ cells in spleen were also significantly increased. They might contribute to the improvement of the disease activity of SLE.
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| Academic Significance and Societal Importance of the Research Achievements |
後天的遺伝子制御によりSLEの病態形成に関与する新規候補microRNAとしてmiR223-3pに着目し、標的遺伝子であるS1PR1の発現制御を介したアポトーシス能への影響等が確認された。SLEは、いまだアンメットメディカルニーズの高い難治性の自己免疫疾患であり、miR223及びS1PR1が新規治療標的となりえる可能性が示唆された。
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