2017 Fiscal Year Final Research Report
Involvement of Activin-A in inflammatory joint disease targeted to IL-17 signaling
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 |
Research Field |
Surgical dentistry
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Research Institution | Kyushu Dental College |
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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Keywords | アクチビン / 破骨細胞 / 顎関節 |
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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Free Research Field |
医歯薬学
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