| Project/Area Number |
16K15655
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
NODA Masaki 東京医科歯科大学, 大学院医歯学総合研究科, 非常勤講師 (50231725)
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| Co-Investigator(Kenkyū-buntansha) |
二藤 彰 鶴見大学, 歯学部, 教授 (00240747)
江面 陽一 東京医科歯科大学, 難治疾患研究所, 准教授 (50333456)
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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 |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 骨芽細胞 / 分子メカニズム / 骨粗鬆症 / イリシン / PTH / ＩＲＩＳＩＮ / 骨形成 / Ｌｇｒ４ / 骨代謝 / メカニカルストレス |
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| Outline of Final Research Achievements |
In order to establish a new strategic foundation for the control of the pathology of osteoporosis, we focused on the molecular mechanism of bone formation promotion based on the interaction with the signal of parathyroid hormone receptor (PPR) coordinated with IRISIN. First, IRISIN was expressed in hard tissues in a time series. As a result, IRISIN expression in hard tissues and its time dependence were clarified. In addition, as an epigenetic control study in hard tissues, we focused on histone methyltransferase G9a to clarify the localization of mRNA and protein. We also revealed that oxidative stress suppressed the level of Lgr4 and the interaction between PTH receptor and beta AdR.
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