2015 Fiscal Year Final Research Report
Basic research of prevention and intervention for congenital cardiac outflow tract defects using animal models
Project/Area Number |
25293238
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Pediatrics
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Research Institution | Keio University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
TSUCHIHASHI TAKATOSHI 慶應義塾大学, 医学部, 共同研究員 (10286528)
MAKINO SHINJI 慶應義塾大学, 医学部, 准教授 (20306707)
UCHIDA KEIKO 慶應義塾大学, 保健管理センター, 講師 (50286522)
YUASA SHINSUKE 慶應義塾大学, 医学部, 准教授 (90398628)
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Co-Investigator(Renkei-kenkyūsha) |
IEDA MASAKI 慶應義塾大学, 医学部, 講師 (70296557)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | 発生・分化 / 発現制御 / 遺伝子 / 循環器・高血圧 / 再生医学 |
Outline of Final Research Achievements |
Using the murine model, we identified that the expression of a neurovascular guiding molecule, Sema3C, is regulated positively by Foxc1 and Foxc2, and negatively by Tbx1 directly in the second heart field and through Fgf8 which is a downstream effector of Tbx1 in the neural crest, respectively, during development of the cardiac outflow tract. Such dynamic temporo-spatial regulation of Sema3c plays a role in the fine tuning of migration of neural crest cells into the outflow tract to give rise to the septum. We also succeeded in visualization of the development of pulmonary arteries from central to peripheral regions of the lungs using a transgenic mouse model in which the lacZ marker gene was inserted into the genome of IP3R type2. Using this mouse model, we also showed the mechanism of pulmonary vascular abnormality associated with cardiac outflow tract defects and candidates of unknown cis/trans elements that specifically regulate the development of pulmonary arterial smooth muscle.
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Free Research Field |
小児科学
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