| Project/Area Number |
26713053
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
Prosthodontics/ Dental materials science and
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| Research Institution | Okayama University |
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Principal Investigator |
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| Research Collaborator |
KUBOKI TAKUO 岡山大学, 大学院医歯薬学総合研究科, 教授 (00225195)
ONO MITSUAKI 岡山大学, 大学院医歯薬学総合研究科, 助教 (60613156)
OSHIMA MASAMITSU 岡山大学, 大学院医歯薬学総合研究科, 助教 (00548307)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥22,490,000 (Direct Cost: ¥17,300,000、Indirect Cost: ¥5,190,000)
Fiscal Year 2016: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2015: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥15,470,000 (Direct Cost: ¥11,900,000、Indirect Cost: ¥3,570,000)
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| Keywords | 間葉系幹細胞 / 創傷治癒 / 宿主免疫応答 / 内在性幹細胞 / 歯学 / 生体機能 / 免疫学 / 再生医療 / 宿主幹細胞 / 宿主間葉系幹細胞 / 炎症 / 組織再生 |
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| Outline of Final Research Achievements |
In this study, we investigated the mechanism of stem cell accumulation in regeneration site during wound healing process. In the mouse wound healing model, host mesenchymal stem cell accumulation was detected in 1 day after surgery. By using cDNA micro-array analysis, TNFa was detected as one of the stem cell accumulation factor. Thus, we confirmed the effect of TNFa on stem cell function including, cell proliferation, mobilization, immune-modulatory property. While TNFa could inhibit the cell proliferation, cell mobilization was strongly up-regulated. Furthermore, immune-modulatory property was, which was evaluated FASL expression, totally up-regulated. These results indicated that TNFa could stimulate host stem cell function and cause immune tolerance in wound healing site.
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