| Project/Area Number |
24592270
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Oita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIOKA Hidekatsu 大分大学, 医学部, 教授 (00222430)
SASAKI Takako 大分大学, 医学部, 助教 (30133193)
OKAMOTO Osamu 大分大学, 医学部, 客員研究員 (40284799)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 軟骨 / 転写 / コラーゲン |
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| Outline of Final Research Achievements |
We investigated the proximal promoter of mouse Col11a1 and Col27a1 gene in chondrocytes.In Col27a1 gene, oligo-Capping Race analysis revealed that mouse Col27a1 gene has two alternative splicing variants in chondrocytes. Transient transfection experiments indicated that the proximal promoter activity was from -586 to -445 in the downstream promoter, and was from -310 to +1 in the upstream promoter. In Col11a1 gene, cell transfection experiments exhibited the suppression of the promoter activity without NF-Y binding sequence. Furthermore, dominant-negative NF-Y inhibited the promoter activity. In addition, luciferase assays exhibited that GC rich sequence is a critical elements. Overexpression of Sp1 was significantly increased, and knockdown of Sp1 was suppressed the expression of endogenous transcript of Col11a1 gene. Taken together, these results indicate that the transcription factor NF-Y and Sp1 upregulates the proximal promoter activity of mouse Col11a1 gene in chondrocytes.
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