| Project/Area Number |
16K20605
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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 |
Surgical dentistry
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
MITSUGI SHO 九州歯科大学, 歯学部, 助教 (00636920)
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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: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | アクチビン / 破骨細胞 / 顎関節 / ATDC5 / 軟骨細胞 / 歯学 / シグナル伝達 / 細胞・組織 / 発現制御 |
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| Outline of Final Research Achievements |
Prior to the elucidation of the modulatory effects on inflammatory joint disease by IL-17, the effect of activin-A alone on osteoclast differentiation was examined.
RANKL-induced osteoclast differentiation, actin ring formation, and bone resorption activity were significantly enhanced by activin-A. Furthermore, activin-A enhanced RANKL-induced expression of nuclear factor of activated T cell cytoplasmic 1 (NFATc1), a key regulator of osteoclastogenesis, thereby increasing osteoclastogenesis-related marker gene expression, including cathepsin K, OC-STAMP, MMP 9. Pre-treatment of the cells with a specific inhibitor of SMAD2/3 attenuated the activin-A-induced expression of NFATc1 and co-immunoprecipitation assay revealed that treatment with activin-A increased physical interaction of phosphorylated-c-fos and phosphorylated-SMAD2 protein induced by RANKL. These results suggest that activin-A enhances RANKL-induced osteoclastformation mediated by interaction of c-fos and SMAD2/3.
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