Development of the treatment for cartilage regeneration by a prostanoid signal-acting material
| Project/Area Number |
16390437
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Kyoto University |
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Principal Investigator |
TOGUCHIDA Junya Kyoto University, Institute for Frontier Medicine, Professor, 再生医科学研究所, 教授 (40273502)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Takashi Kyoto University, Graduate School of Medicine, Professor, 大学院・医学研究科, 教授 (10201675)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥13,500,000 (Direct Cost: ¥13,500,000)
Fiscal Year 2005: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 2004: ¥9,000,000 (Direct Cost: ¥9,000,000)
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| Keywords | articular cartilage / Prostaglandin E2 / EP2 receptor / mesenchymal stem cell / cartilage regeneration / プロスタグランデインE2 / PGE2 / EP2 / 軟骨修復 / マイクロアレイ |
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| Research Abstract |
The effects of EP2 agonists for the treatment of articular cartilage defects were investigated by in vivo experiments. Full thickness cartilage defects (5mm in diameter and 5mm depth) and surface cartilage defects (5mm in dianeter) were created in the patello-femoral joint surface of the distal portion of femurs of rabbits. Histological examination was performed immediately after the operation, which confirmed the porper procedure to creat intended defects for each model. Treatment was carried out using EP2 agonists slow-releasing materials (PLGA+gelatin gel, 5mm in diameter and 5mm height), which was placed in the defect in the case of full thickness defect model and adjacet to infrapatellar fat pad in the case of surface defect model. The amount of EP2 agonist were either 20mg, 80mg, or 800mg. Animals were sacrified at four weeks after operation, and the defects were examined histologically. In the case of full thickness model, the defect was filled with tissues, which mainly composed of safranion-O negative spindel cells. The proliferation of cartilage cells were observed at the junction facing to residual normal articular cartialge, the amount of which depended on the dose of EP2 agonists. In the surface defect model, the defect was filled with regenerated chondrocytes, which were positive for safaranin-O staining. There were many lacunae containing two cells, indicating the active proliferation of articular chondrocytes. These resultis suggested that PGE2 signal through EP2 stimulated proliferation of articular cartilage cells, and that combined with a proper drug-delivery system, EP2 agonists will be promising therapeutic materials for damaged articular cartilages, which have been regarded not to have a regenerative potency.
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Report
(3 results)
Research Products
(18 results)
