| Project/Area Number |
25462886
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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 |
Functional basic dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
Kubota Satoshi 岡山大学, 医歯(薬)学総合研究科, 教授 (90221936)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIGAWA Masaharu 岡山大学, 大学院医歯薬学総合研究科, 教授 (20112063)
HATTORI Takako 岡山大学, 大学院医歯薬学総合研究科, 助教 (00228488)
NISHIDA Takashi 岡山大学, 大学院医歯薬学総合研究科, 准教授 (30322233)
AOYAMA Eriko 岡山大学, 大学院医歯薬学総合研究科, 助教 (10432650)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | CCN family / CCN2 / CCN3 / fibrosis / cartilage / osteoarthritis / 軟骨 / 再生 / CTGF / NOV / 骨 / 再生医療 / 橋渡し研究 |
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| Outline of Final Research Achievements |
Suspecting a biological diarchy by CCN2 and CCN3, CCN3 was overexpressed in fibrogenic cells. Consequently, the gene expression of profibrotic CCN2 and CCN4 were repressed. Also, overexpression of CCN3 disharmonizing the CCN2/CCN3 balance resulted in obvious delay in the final stage of endochondral ossification. New CCN2 molecular counterparts were identified as well.
Subsequently, in a rat osteoarthritis (OA) rat model, CCN3 that was present in normal articular cartilage was drastically decreased, contrarily to CCN2. Ameliorating effects of CCN3 locally applied to the OA lesion was observed.
Finally, by analyzing the components of platelets as a model of tissue regenerating tools, inclusion of CCN1, CCN3 and CCN5, as well as CCN2, was clarified therein. A CCN cocktail mimicking platelets showed even greater regeneration potential than CCN2 alone, suggesting its clinical utility.
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