2001 Fiscal Year Final Research Report Summary
Effect of tension-stress on gene expression of one and cartilage cells. Molecular mechanism of distraction osteogenesis
| Project/Area Number |
12671413
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | The University of Tokushima |
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Principal Investigator |
YASUI Natsuo The University of Tokushima, School of Medicine, Professor, 医学部, 教授 (00157984)
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| Co-Investigator(Kenkyū-buntansha) |
NAKASE Takanao Osaka University Medical School, Assistant Professor, 大学院・医学系研究科, 助手 (00283755)
TAKADA Shinjiro The University of Tokushima, School of Medicine, Assistant Professor, 医学部・附属病院, 助手 (20284292)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Mechanical stress / Distraction osteogenesis / Bone formation / Chondrocytes |
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| Research Abstract |
We have recently established a rat model of distraction osteogenesis, and demonstrated that the mode of ossification changed from endochondral to intramembranous via transchondroid bone formation depending on the stage of distraction. The present -study was designed to investigate the effect of mechanical tension-stress on gene expression of bone morphogenetic protein (BMP)-2 and BMP-4 and Runx2 by the cells involved in distraction osteogenesis. Runx2 is a transcription factor that exists in the downstream of BMPs. It bind to DNA through Runt- domain and plays an fundamental role in osteoblast differentiation. Northern blot analysis and in situ hybridization showed that Runx2 gene, as well as BMP-2 and BMP-4 genes, were highly expressed by the chondroid cells exposed to mechanical tension-stress. These cells seemed to switch their collagen phenotype from type II to type I to differentiate from chondroid cells into osteoblasts. After completion of distraction, none of BMP-2, BMP-4 and Runx2 were detected withm the lengthened segment. The present results suggest that abundant gene products of BMP-2, BMP-4 could induce abundant Runx2 and enhance the in situ bone formation by paracrine and autocrine mechanism.
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