Systemic delivery of microRNA for therapy of IBD
| Project/Area Number |
16K15590
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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 |
General surgery
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 炎症性腸疾患 / マイクロRNA / 樹状細胞 / スーパーアパタイト / miR-29 / DDS / 核酸 / 全身デリバリー / 治療薬探索 |
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| Outline of Final Research Achievements |
Although anti-TNF antibodies and immunosuppressive agents can achieve remission, recurrence is common in inflammatory bowel disease (IBD). Accordingly, novel therapeutic strategies are needed.The aim of this study was to establish microRNA-based therapy in an IBD model. For this purpose, we used microRNA-29 (miR-29) and a super carbonate apatite (sCA) nanoparticle as a drug delivery system. Injection of sCA-miR-29a-3p or -29b-3p into the tail veins of mice markedly prevented inflammation due to dextran sulfate sodium (DSS)-induced colitis. We found that sCA-negative control miR predominantly accumulated in CD11c+ dendritic cells (DCs) in the inflamed epithelium. RNA sequencing and Ingenuity Pathway Analysis revealed that miR-29a or -29b could inhibit interferon signaling pathways. Injection of sCA-miR-29b efficiently targeted CD11c+DCs in the inflamed mucosa. The present study showed that systemic delivery of miR-29 prevented DSS-induced colitis.
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Report
(3 results)
Research Products
(1 results)
