| Project/Area Number |
25670629
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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 | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Takeyuki 東京大学, 医学部附属病院, 助教 (00583121)
SAWADA Ryoko 東京大学, 医学部附属病院, 特任研究員 (30648308)
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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 |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 変形性関節症 / 関節軟骨 / 低酸素 / オートファジー / 整形外科学 / autophagy / chondrocyte / hypoxia |
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| Outline of Final Research Achievements |
We observed mouse primary chondrocytes with hypoxia or starvation stress, and found that stabilization of transcription factor HIF1A participated as one of the trigger of the induction of expression and activity of the autophagic factor known in the other cells. Knockout of Hif1a in the isolated joint cartilage cells from Hif1a-flox mouse introduced Cre recombinase with an adenovirus, canceled activation of the autophagy partially, but enhanced the cell death at the same time and the expression of cartilage substrate degrading enzymes such as Mmp13. This mechanism might play a role of making the pathological condition such as osteoarthritis.
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