| Project/Area Number |
25462876
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Tokai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Minoru 東海大学, 医学部, 教授 (10146706)
渡部 聡 国立研究開発法人農業生物資源研究所, ゲノム研究センター・家畜ゲノム, 主任研究員 (80391572)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 22q11.2欠失症候群 / DGCR2 / Sez12 / ノックアウトマウス / 頭蓋底軟骨結合 / TGF-beta / 顎顔面骨格形成 / ノックインGFP / 軟骨細胞分化 / Dgcr2 / TGF-βシグナル / BMPシグナル / 顎形態形成 / Tbx1 / BMP |
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| Outline of Final Research Achievements |
It has been suggested that the DGCR2 gene plays a role in the pathogenesis of 22q11.2 deletion syndrome. To analyze its function, we used our Sez12-knock-out/EGFP-knock-in mice (Sez12-KO mice). At weaning, approximately 50% of Sez12-KO mice showed mild skeletal abnormalities. Skeletal analyses revealed maxillofacial malformation in Sez12-KO mice around 6-week-old. In histology, the knock-in EGFP was expressed significantly in cartilage tissues and especially in hypertrophic chondrocytes, whose sparseness was observed in cranial base of Sez12-KO mice. Here we examined the Sez12 gene function with the primary cultured chondrocytes from Sez12-KO mice. When TGF-beta was applied, the Sez12-KO chondrocytes changed to fibroblast-like cell shape with expression of type I collagen. Our results suggest that Sez12 plays a role for maintenance and/or survival of hypertrophic chondrocytes by regulating TGF-beta signaling.
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