2003 Fiscal Year Final Research Report Summary
Tissue Engineering with leg lengthening system : involvement of reactive oxygen species.
| Project/Area Number |
13671551
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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 | Kinki University |
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Principal Investigator |
HAMANISHI Chiaki Kinki Univ., School Med., Dept. Orthop.Surg., Professor, 医学部, 教授 (00164921)
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| Co-Investigator(Kenkyū-buntansha) |
MORI S. Kinki Univ., School Med., Dept. Orthop.Surg., Assistant, 医学部, 助手 (80351584)
OTANI K. Kinki Univ., School Med., Dept. Orthop.Surg., Lecturer, 医学部, 講師 (20258031)
FUKUDA K. Kinki Univ., School Med., Dept. Orthop.Surg., Professor, 医学部, 教授 (50201744)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Chondrocyte / Mechanical stress / nitric oxide / 骨芽細胞 |
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| Research Abstract |
Many tissues or organs including bone and joint adopted their morphology under the influence of the environmental mechanical loading. The purpose of this study is to solve this mysterious process and apply it for therapeutic aspect as tissue engineering. We introduce the distraction osteogenesis, which afford to correct the deformity and lengthen the limb. Although mechanical stretch on bone, tendon and vessel is possible to apply, lag period in the bone maturation is necessary. To improve this system, we investigate the role of reactive oxygen species(ROS) under the influence of mechanical stress.
We used in vivo model of leg-lengthening *and found the characteristic morphology, such as the invasion of endothelial cells and apoptosis of mesenchymal cells. We first focused on the distribution of apoptosis of the osteoblast in this model. Recent observations revealed the significant role of ROS in ischemia-reperfusion induced cell apoptosis. We then examine the effect of mechanical stress on generation of the ROS and apoptosis of osteoblast. Cyclic tensile stretch loaded oh these cells clearly enhanced ROS synthesis in a time-and magnitude-dependent fashion. The disruption of micro filaments abolished the stress-induced ROS synthesis. Rotenone, an inhibitor of the mitochondrial electron transport chain, enhanced stress-induced ROS synthesis. These data suggest that actin filament and mitochondria are involved in this action.
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