Mechanism investigation of signal transduction on scar tissue formation of palatal mucosa
| Project/Area Number |
15592157
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
BABA Yoshiyuki Tokyo Medical and Dental University, Graduate School of Medical and Dental Science, Division of Mxillofacial Orthognathics, Instructor, 大学院・医歯学総合研究科, 助手 (70251535)
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| Co-Investigator(Kenkyū-buntansha) |
ICHIJO Hidenori The University of Tokyo, Graduate School of Pharmaceutical Science, Division of Cell Signaling, Professor, 大学院・薬学系研究科, 教授 (00242206)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | palatal mucosa / scar tissue / organ culture / alpha-smooth muscle / FGFR / TGF-β1 / TGF-β1 |
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| Research Abstract |
The purpose of studies was, 1.establishment of the organ culture system for the investigation of rat palatal wound hearing model, and, 2.mechanism investigation of signal transduction of SMAD and ASK-1 mediated differentiation from fibroblasts into myofibroblasts.
1.In order to establishing an in vitro organ culture model, after excision of palatal mucoperiosteum, explants from the developing immature scar tissue and from the normal palatal mucosa were used to observe myofibroblasts in vivo. The optimal culture condition was confirmed that xplants were cultured in the gas-liquid interface in serum-free Waymouth's MB 752/1 medium and in a humid atmosphere containing 55%O2/5%CO2 at 37 ℃. These results demonstrate that the established model provides a useful in vitro experimental tool for further investigation.
2.Fibroblast growth factors (FGFs) regulate cell growth and differentiation and play crucial roles in the process of tissue repair and remodeling. We have previously shown that basic FGF is widely expressed at the injured site. Since the presence of FGF receptors (FGFRS) determines cellular responsiveness, we examined the localization of FGFR1, FGFR2 and FGFR3 expression by immunohistochemistry throughout the repair of full thickness excisional wounds up to 28 days after wounding. Strong expression of FGFR1 was observed in the nuclei of myofibroblasts, which are characterized by α-smooth muscle (α-SM) actin expression. The weak expression of FGFR2 was also observed in the nuclei of myofibroblasts. In contrast, there was no staining for FGFR3 in fibroblasts through the wound healing process. In addition, transforming growth factor-β1 (TGF-β1), a potential inducer of myofibroblasts, enhanced the expression of FGFR1 and FGFR2 in the nuclei of palatal fibroblasts in vitro. These findings suggest that FGFR1 and FGFR2 in myofibroblasts may be responsible for the signal transduction of FGF during the wound healing process.
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Report
(3 results)
Research Products
(6 results)
