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KAKEN_25293238seika.pdf
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Title |
Title |
動物モデルを用いた先天性心臓流出路異常の予防と新たな治療への基礎的研究
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Kana |
ドウブツ モデル オ モチイタ センテンセイ シンゾウ リュウシュツロ イジョウ ノ ヨボウ ト アラタナ チリョウ エノ キソテキ ケンキュウ
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Dobutsu moderu o mochiita sentensei shinzo ryushutsuro ijo no yobo to aratana chiryo eno kisoteki kenkyu
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Basic research of prevention and intervention for congenital cardiac outflow tract defects using animal models
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山岸, 敬幸
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Kana |
ヤマギシ, ヒロユキ
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Romanization |
Yamagishi, Hiroyuki
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Affiliation |
慶應義塾大学・医学部・准教授
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Research team head
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科研費研究者番号 : 40255500
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土橋, 隆俊
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ツチハシ, タカトシ
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Romanization |
Tsuchihashi, Takatoshi
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慶應義塾大学・医学部・共同研究員
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Research team member
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科研費研究者番号 : 10286528
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牧野, 伸司
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マキノ, シンジ
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Makino, Shinji
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Affiliation |
慶應義塾大学・医学部・准教授
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Research team member
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科研費研究者番号 : 20306707
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内田, 敬子
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ウチダ, ケイコ
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Uchida, Keiko
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慶應義塾大学・保健管理センター・講師
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Research team member
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科研費研究者番号 : 50286522
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湯浅, 慎介
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ユアサ, シンスケ
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Yuasa, Shinsuke
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Affiliation |
慶應義塾大学・医学部・准教授
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Research team member
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科研費研究者番号 : 90398628
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家田, 真樹
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イエダ, マサキ
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Romanization |
Ieda, Masaki
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Affiliation |
慶應義塾大学・医学部・講師
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Research team member
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科研費研究者番号 : 70296557
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2016
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科学研究費補助金研究成果報告書
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2015
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Abstract |
マウスモデルを用いて, 心臓流出路発生における分泌因子Sema3Cの発現が転写因子Foxc1/2に活性化され, 二次心臓領域では転写因子Tbx1に直接的に, 心臓神経堤細胞ではTbx1の下流分泌因子Fgf8を介して間接的に抑制されることを明らかにした。このダイナミックな発現制御により, 心臓神経堤細胞の正常な遊走が誘導され, 流出路中隔が形成される。また, IP3R2型の発現部位をLacZで標識するマウスにより中枢から末梢にかけての肺動脈発生の可視化に成功し, このマウスモデルを利用して心臓流出路異常に伴う肺血管発生異常の機序を明らかにし, 肺動脈平滑筋に特異的な未知の発現制御配列と制御因子の候補を特定した。
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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研究種目 : 基盤研究(B)(一般)
研究期間 : 2013~2015
課題番号 : 25293238
研究分野 : 小児科学
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