2017 Fiscal Year Final Research Report
Demonstration of molecular mechanism of steroid-induced osteonecrosis
Project/Area Number |
15K10497
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Orthopaedic surgery
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Research Institution | Kanazawa Medical University |
Principal Investigator |
ICHISEKI Toru 金沢医科大学, 医学部, 准教授 (30307631)
|
Co-Investigator(Kenkyū-buntansha) |
岡崎 俊朗 金沢医科大学, 医学部, 教授 (40233308)
上田 善道 金沢医科大学, 医学部, 教授 (50271375)
植田 修右 金沢医科大学, 医学部, 助教 (10759583)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Keywords | 特異的スフィンゴミエリン合成酵素マウス / ステロイド / 血管内皮細胞 / 骨細胞 / 骨芽細胞 / SM-1 / SM-2 / 遺伝子改変マウス |
Outline of Final Research Achievements |
Twelve to 24 hours after the development of angiogenesis-osteogenesis coupling injury osteocytes were thought to have become necrotic. Also, bone as compared with heart, liver, kidney, and blood vessels was shown to be more susceptible to oxidative stress which is the instigator of necrosis, and showed a significantly greater decrease in antioxidant enzyme and mitochondrial function after steroid administration. The results of the histological study on bone tissue formation in the SMS-1/SMS-2 double knockout mouse revealed the presence of bone tissue hypoplasia and defective calcification due to osteoblast disarrangement in the long bone and spinal growth plate, implicating bone metabolism, especially sphingomyelin in osteoblast function.
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Free Research Field |
医歯薬学
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