| Project/Area Number |
17390486
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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 |
Morphological basic dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
TAKATA Takashi Hiroshima University, Graduate School of Biomedical Sciences, Professor (10154783)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAUCHI Mutsumi Hiroshima University, Graduate School of Biomedical Sciences, Associate Professor (50169265)
KUDO Yasusei Hiroshima University, Graduate School of Biomedical Sciences, Assistant Professor (50314753)
OGAWA Ikuko Hiroshima University, Hiroshima University Hospital, Associate Professor (70136092)
KITAGAWA Masae Hiroshima University, Hiroshima University Hospital, Assistant Professor (10403627)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥16,890,000 (Direct Cost: ¥15,600,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2007: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2006: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2005: ¥7,300,000 (Direct Cost: ¥7,300,000)
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| Keywords | ameloblastin / synthetic peptide / bone regeneration / osteoblast / bone defect / p38 / CD68 / alkaline phosphatase / 骨 / 再生 / エナメル蛋白 / ペプチド / 担体 / 骨折 / レセプター / ゼラチン |
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| Research Abstract |
To determine whether synthetic peptide of the N-terminal of ameloblastin as a novel regenerative agent for bore defect, we achieved in vitro and in vivo analyses and obtained the following results.
1. To determine the ameloblastin fragment with the most active biological effects on osteoblastic cells, we examined activities of alkaline phosphate and calcification of osteoblastic cell line, MC3T3-E1, after treatment of various lengths of N-terminal area of ameloblastin. It was show that the highest inductive effects were seem when the cells treated with 16 amino acids (VPFFPQQSGTPGMASL) at N-terminal of ameloblastin (16N).
2. To examine the signaling pathway of 16N in osreoblasts, expression of MAPK in MC3T3-E1 cells after the treatment of 16N. Phosphotylation of p38 was seen in the cells.
3. To recognize the receptor of 16N, we transfected cDNA encoding 16N into MC3T3-E1cells. A vector with the sequence of secretion could induce high alkaline phosphatase activity in MC3T3-E1 cells, while a vector without the sequence of secretion didn't induced. It was, therefore speculated that the receptor of 16N may present on the surface of MC3T3-E1 cells.
4. Although identification of the membrane located receptor was not accomplished, CD63was detected on the cell membrane of MC3T3-E1 cells and suspected as a potential receptor of 16N.
5. In vivo studies with different bone defect models showed regeneration promoting effects on 16N. These findings indicate that 16N can be used for novel agent promoter of bone healing
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