The Sonic Hedgehog signaling pathway involves duodenal atresia in patients with Down syndrome
Project/Area Number |
24591517
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | Oita University |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
Keywords | Down症候群 / 十二指腸閉鎖 / Sonic Hedgehog経路 / アミロイドβ / PTCH1 / ソニックヘッジホッグ経路 / Sonic Hedgehog pathway / Duodenal atresia |
Outline of Final Research Achievements |
We examined relevance of the Sonic Hedgehog pathway for the duodenal atresia in Down syndrome because its signaling plays an important role in development of the gastrointestinal tract. The subjects were used plasma and leukocytes for material specimen from 21 patients of Down syndrome included a patient with duodenal atresia and 10 healthy individuals. Amyloid β protein levels were elevated 1.67 fold high value in patients with Down syndrome as compared with healthy controls by ELISA. Furthermore, overexpression of PTCH1 and GLI3 were immunohistologically confirmed at a lesion of duodenal atresia in a Down syndrome patient. There is no correlation in the PTCH1 mRNA expression level and the amount of PTCH1 proteins. Western blot analysis revealed that the PTCH1 proteins became high levels when amyloid β proteins was high value in plasma of Down syndrome. We suggested that the duodenal atresia in Down syndrome might be caused by high expression of PTCH1 protein.
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Report
(4 results)
Research Products
(1 results)