| Project/Area Number |
23792034
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatric surgery
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| Research Institution | Nihon University |
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Principal Investigator |
KANEDA Hide 日本大学, 医学部, 専修指導医 (30598967)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 先天性消化器疾患学 / 脱分化脂肪細胞 / DFAT / 肛門括約筋障害 / cardiotoxin / 肛門内圧測定 / 肛門内圧 / 肛門括約筋 |
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| Research Abstract |
I found significantlyα-Smooth muscle actin (αSMA) positive cell at the smooth muscle differentiation medium compared with the control (5%FCS), cultured rat DFAT with the smooth muscle differentiation medium (5%FCS, TGFβ5ng/ml). To confirm whether rat DFAT have possibility of smooth muscle and skeletal muscle differentiation in vivo, I producted anal canal (it consists of smooth muscle and skeletal muscle) dysfunction rat model using cardiotoxin (CTX). Green fluorescence protein (GFP)-labeled DFAT or PBS were injected into para-anal canal tissue. Immunohistochemistry revealed that inner smooth muscle and external striated muscle layers in anal canal showed atrophy or necrosis in the control group, whereas DFAT transplantation led an increase of smoothe muscle and striated muscle mass with variable fiber orientation. GFP-labeled DFAT model showed a decrease of inflammatory cells in HE stain. DFAT cell transplantation resulted in a significant improvement of anal canal pressure, compared with control. DFAT cell transplantation promotes anal canal muscle regeneration and improves anal canal pressure.
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