| Project/Area Number |
26462303
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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 | Kumamoto University |
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Principal Investigator |
Mizuta Hiroshi 熊本大学, 大学院生命科学研究部(医), 教授 (60174025)
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| Co-Investigator(Kenkyū-buntansha) |
廣瀬 隼 熊本大学, 医学部附属病院, 准教授 (40433007)
岡元 信和 熊本大学, 大学院生命科学研究部(医), 助教 (70600162)
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| Co-Investigator(Renkei-kenkyūsha) |
OYADOMARI Seiichi 徳島大学, 疾患ゲノム研究センター, 教授 (90502534)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 小胞体ストレス / 軟骨細胞機能 / アポトーシス / 機械的刺激 / 低酸素 / AGEs / メカニカルストレス |
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| Outline of Final Research Achievements |
This study showed that endoplasmic reticulum (ER) stress was induced by long-term excessive mechanical stress, resulting decrease of anabolic function, increase of catabolic function, and apoptosis in cultured chondrocytes. We also confirmed this finding in conditions mimicking the intra-articular environments in elderly patients with osteoarthritis. Furthermore, it was suggested that ATF6α, the ER stress sensor protein, may reduce the negative effects by mechanical stress such as decrease of anabolic function, increase of catabolic function, and increase of apoptosis in chondrocytes.
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