| Project/Area Number |
19K24124
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Multi-year Fund |
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| Review Section |
0907:Oral science and related fields
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| Research Institution | Nagasaki University |
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Principal Investigator |
QIN Xin 長崎大学, 医歯薬学総合研究科(歯学系), 特任研究員 (60846559)
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| Project Period (FY) |
2019-08-30 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | osteoporosis / bone formation / bone resorption / knockout mice / glucocorticoid / unloading / bone development / Osteoporosis |
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| Outline of Research at the Start |
Fkbp5 have been shown to be involved in physiological stress response. However, there is no report about the function of Fkbp5 in bone. This is the first study to use Fkbp5 knock out mice for further understanding the molecular mechanism of GC-induced osteoporosis.
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| Outline of Final Research Achievements |
We identified Fkbp5 as an unloading-induced molecule in osteoblasts and osteocytes, and collected RNA from the osteoblast-enriched fraction from wild-type and Fkbp5 knockout mice with or without GC treatment, examined osteoblast marker gene expressions. We performed microarray analysis by using osteoblast and osteocyte fractions. The expression of the selected genes by gene annotation and pathway analyses was analyzed by real-time reverse transcription (RT)-PCR.
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| Academic Significance and Societal Importance of the Research Achievements |
この研究の目的は、無負荷状態でのFkbp5の役割を特定することにより、廃用性骨粗鬆症における骨形成障害の分子メカニズムを解明し、GC誘発性骨粗鬆症における骨形成障害の原因となる分子を特定することである。また、 Fkbp5ノックアウトマウスを使用して、GC誘発性骨粗鬆症におけるRunx2タンパク質の減少のメカニズムを明らかにする。 Fkbp5は廃用性骨粗鬆症において新しい機能を持つため、廃用性骨粗鬆症の分子メカニズムを明らかにする珍しい研究である。
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