Pathological analysis of Apert syndrome mice model in submandibular gland
| Project/Area Number |
15K20968
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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 |
Orthodontics/Pediatric dentistry
Morphological basic dentistry
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
Morita Jumpei 九州歯科大学, 歯学部, 助教 (50737046)
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| Research Collaborator |
YAMAJI Kojiro
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| Project Period (FY) |
2015-04-01 – 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 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | Apert症候群 / 唾液腺 / 先天性疾患 / 矯正歯科 / 線維芽細胞増殖因子受容体 |
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| Outline of Final Research Achievements |
Apert syndrome is characterized by craniosynostosis and severe bony syndactyly of the hands and feet. The cause of Apert syndrome is a single nucleotide substitution mutation (S252W or P253R) in fibroblast growth factor receptor 2 (FGFR2). Clinical experience suggests increased production of saliva by Apert syndrome patients, but this has not been formally investigated. Using Apert syndrome mice model, we investigated the role of FGFR2 in SMGs and analyzed the SMG pathology of Apert syndrome.
In Ap mice, the number of lobules was small and the average area of lobules and the parenchyma occupancy rate were large compared with controls. Ap mice showed morphological changes in the SMGs, which are likely to be caused by gain-of-function of FGFR2, suggesting the possibility that epithelial cell proliferation is enhanced.
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Report
(3 results)
Research Products
(4 results)
