Research of signals involved in development of the anorectum by model mice of anorectal malformations
Project/Area Number |
25861665
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Pediatric surgery
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Research Institution | Chiba University |
Principal Investigator |
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Project Period (FY) |
2013-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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Keywords | 直腸肛門奇形 / Wnt5aコンディショナルノックアウトマウス / 肛門括約筋 / 肛門括約筋群 / Wnt5aコンディショナルノックアウト |
Outline of Final Research Achievements |
We examined the role of Wnt5a for anorectal malformations and development of the anal sphincter by Wnt5a conditional knock-out mouse. 0.05g/maternal weight of Tamoxifen induced necessarily the phenotype. When tamoxifen dosed at enbryonal day 8, the anorectal malformation of the fetus was induced. When tamoxifen dosed after enbryonal day 9, anal opening was normal. The maldevelopment of the elongation of the cloacal plate caused anorectal malformations embryologically. The induction of Wnt5a elongated the cloacal plate. It was shown that Wnt5a decided the phenotype of anorectal malformations at the early stage of the fetus. But wnt5a was not directly concerned with the pathogenesis of an anal sphincter.
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Report
(5 results)
Research Products
(3 results)