| Project/Area Number |
21592597
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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 |
Orthodontic/Pediatric dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
TANAKA Eiji The University of Tokushima, 大学院・ヘルスバイオサイエンス研究部, 教授 (40273693)
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| Co-Investigator(Kenkyū-buntansha) |
KINOUCHI Nao 徳島大学, 病院, 助教 (30457329)
KAWAI Nobuhiko 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (40437588)
HIASA Masahiro 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (90511337)
TOMITA Yuko 徳島大学, 病院, 医員 (70380095)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
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| Keywords | 歯科矯正学 / 創傷治癒 / 口蓋粘膜 / Smad3 / 瘢痕形成 / siRNA / Smad3拮抗薬 |
|---|
| Research Abstract |
The purpose of this study was to investigate the role of TGF-・Smad3 signaling in palatal wound healing using Smad3-deficient (Smad3^<-/->) mice. Histological examination showed that wound closure was accelerated by promoting proliferation of epithelium and dermal cells in Smad3^<-/-> mice compared with wild-type (WT) mice. Macrophage/monocyte infiltration at wounded region in Smad3^<-/-> mice was decreased in parallel with the diminished production of TGF-β1, MCP-1 and MIP-・compared with WT mice. Fibrocytes, expressing hematopoietic surface marker and fibroblast products, were recruited and produced ・-smooth muscle actin in WT mice, but were not observed in Smad3^<-/-> mice. These results suggest that TGF-β/Smad3 signaling may play an important role in the regulation of palatal wound healing.
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