| Project/Area Number |
17H06885
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
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| Research Collaborator |
TAKIGAWA Masaharu 岡山大学, 医歯薬学総合研究科, 教授 (20112063)
SATO Yasufumi 東北大学, 加齢医学研究所, 教授 (50178779)
KUBOTA Satoshi 岡山大学, 医歯薬学総合研究科, 教授 (90221936)
AOYAMA Eriko 岡山大学, 医歯薬学総合研究科, 助教 (10432650)
SUZUKI Yasuhiro 東北大学, 加齢医学研究所, 助教 (60332277)
HATTORI Takako 岡山大学, 医歯薬学総合研究科, 助教 (00228488)
YOSHIDA Shoko 岡山大学, 大学病院, 医員 (00616047)
SASAKI Akira 岡山大学, 医歯薬学総合研究科, 教授 (00170663)
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| Project Period (FY) |
2017-08-25 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | CCN2 / VASH1 / 内軟骨性骨化 / 軟骨 |
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| Outline of Final Research Achievements |
The aim of this study is to investigate a novel regulatory mechanism of endochondral ossification by CCN2 and VASH1. We found that both CCN2 and VASH1 were localized in the hypertrophic chondrocyte layer. CCN2-silencing in chondrocytes reduced the expression of VASH1 and increased apoptotic cells, and its increase was suppressed by a ROS inhibitor, N-acetyl-L-cysteine. These results suggest that up-regulation of CCN2-VASH1 axis may suppress the elevation of ROS level that causes chondrocyte cell death/apoptosis and keep hypertrophic chondrocytes surviving until the terminal stage of chondrogenic differentiation.
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| Academic Significance and Societal Importance of the Research Achievements |
学術的意義：本研究により、未だにほとんど解明されていない「内軟骨性骨化の最終段階―軟骨から骨への転化段階」の調節メカニズムの一端を解明する成果が生み出された。
社会的意義：本研究により、骨・軟骨形成に異常をきたす疾病の原因・病態究明、治療法開発につながる成果が生み出された。
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