| Project/Area Number |
25861745
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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 |
Morphological basic dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
TERAMACHI Jumpei 徳島大学, ヘルスバイオサイエンス研究部, 助教 (20515986)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 骨髄ストローマ細胞 / TAF12 / 活性化ビタミンD3 / RANKL / 破骨細胞 / 活性型ビタミンD3 |
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| Outline of Final Research Achievements |
We previously found that transcription initiation factor TFIID subunit 12 (TAF12), a coactivator of the vitamin D receptor is increased in the osteoclast precursors or bone marrow stromal cells. However the role of increased TAF12 on osteoclastogenesis is unclear. Therefore, we aimed to clarify the role of TAF12 in bone marrow stromal cell support of osteoclast formation and function. TNF-α and IL-6 upregulates the expression of TAF12. Increased TAF12 expression induces hyper-sensitivity to 1,25-(OH)2D3. RANKL expression and osteoclast formation were induced at very low levels of 1,25-(OH)2D3. In immunoprecipitation assay, TAF12 and ATF7 physically interact in stromal cells. Knockdown of TAF12 in IL-6-induced TAF12 expressing stromal cell decreased hyper-sensitivity to 1,25-(OH)2D3; as well as RANKL expression and osteoclast formation. These results show that TAF12 contributes to the hypersensitivity of bone marrow stromal cells to 1,25-(OH)2D3 in inflammatory bone disease.
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