The development of novel therapeutic drug for periontitis targeting epgenetic regulation of TLR2
| Project/Area Number |
16K20675
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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 |
Periodontology
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| Research Institution | Kyushu University |
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Principal Investigator |
Tanaka Urara 九州大学, 大学病院, 助教 (50734993)
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Decitabine / 歯周炎モデルマウス / DNAメチル化 / 歯周炎 / TLR2 / エピジェネティックス / P. gingivalis |
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| Outline of Final Research Achievements |
The purpose of this study was to develop a novel therapeutic drug for periodontitis targeting epigenetics.
We observed severe bone loss in the ligature induced periodontitis model in mice and Decitabine significantly inhibited the bone loss. We found that the treatment with Decitabine significantly reduced osteoclasts both in vivo and in vitro and up-regulated the anti-inflammatory cytokines (IL-10 and TGF-β) in vitro. Next, we focused on Kruppel-like Factor 2 (KLF2) which is a transcription factor regulating inflammation. As the results, Decitabine increased KLF2 and KLF2 up-regulated the transcriptional activity of CCAAT/enhancer binding protein beta (CEBPB) and the anti-inflammatory cytokines IL-10 and TGF-β. We concluded that Decitabine inhibits alveolar bone loss by limiting osteoclastogenesis in mice and shows KLF2 can regulate that. Taken together, Decitabine may have utility in treating chronic inflammatory periodontal disease in humans.
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Report
(3 results)
Research Products
(14 results)
