| Project/Area Number |
11670746
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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 |
Pediatrics
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| Research Institution | Niigata University |
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Principal Investigator |
UCHIYAMA Makoto School of Medicine, Niigata University, Prof., 医学部, 教授 (80108050)
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| Co-Investigator(Kenkyū-buntansha) |
SATOKATA Ichiro Niigata Univ., Medical Hospital, Lecturer, 医学部・附属病院, 講師 (70170800)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | osteoblast / Msx1 / Msx2 / BMP / Sox9 / 軟骨細胞 / BMP-2 |
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| Research Abstract |
To clarify the function of homeobox genes Msx1 and Msx2 in osteoblast and chondrocyte differentiation, we analyzed the bone formation of Msx2-deficient and Msx1, Msx2- double deficient mice. Msx2-deficient mice have defects of skull ossification and persistent calvarial foramen. This phenotype results from defective proliferation of osteoprogenitors at the osteogenic front during calvarial morphogenesis and closely resembles that associated with human MSX2 haploinsufficiency in parietal foramina. Msx2-deficient mice also have defects in endochondral ossification. Post-natal deficits in expression of marker genes for bone and catilage differentiation indicate that Msx2 is required for both osteogenesis and chondrogenesis. We also established and characterized Msx1-/-, Msx2-/-, Msx1-/- ; Msx2+/-, Msx1+/- ; Msx2-/-, and Msx1-/- ; Msx2-/- cell lines from both mutant calvaria and body wall. Osteoblastic maturation stimulated by recombinant human BMP-2 was reduced in these mutant cell lines.
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