| Project/Area Number |
26670666
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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 | Hiroshima University |
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Principal Investigator |
OCHI MITSUO 広島大学, その他部局等, 学長 (70177244)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAKI SHIGERU 広島大学, 病院, 講師 (10392490)
KAMEI NAOSUKE 広島大学, 病院, 講師 (70444685)
NAKASA TOMOYUKI 広島大学, 病院, 病院助教 (60467769)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | マイクロRNA / 磁気ターゲッティング / 難治性骨折 |
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| Outline of Final Research Achievements |
It is difficult to achieve bone union for refractory fracture cases with a non- invasive technique. MicroRNAs (miRNAs) are short, non-coding RNAs that act as repressors of gene expression at the level of post transcriptional regulation. The aim of this study was to identify miRNA which play an important role in osteogenesis, and acceleration of bone union by regulating identified miRNA in rat refractory fracture model. miR-222 was identified by microarray analysis during osteogenesis. Inhibition of miR-222 promoted osteogenesis and over-expression of miR-222 inhibited osteogenesis from human mesenchymal stem cells in vitro. miR-222 inhibitor was administered into the fracture site in rat refractory fracture model. Bone union at the fracture site was achieved in the miR-222 inhibitor administration by confirming radiographic and histological evaluation. Local administration of miR-222 inhibitor could accelerate bone healing through enhancing osteogenesis in the rat refractory model.
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