| Project/Area Number |
26293249
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
赤池 徹 東京慈恵会医科大学, 医学部, 助教 (20647101)
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| Co-Investigator(Renkei-kenkyūsha) |
Morita Kiyozou 東京慈恵会医科大学, 心臓外科, 教授 (70174422)
Urashima Takashi 東京慈恵会医科大学, 小児科, 講師 (20338875)
Nakamura Tomoyuki 関西医科大学, 医学部, 教授 (20362527)
Aoki Hiroki 久留米大学, 循環器病研究所, 教授 (60322244)
Akaike Toru 東京慈恵会医科大学, 細胞生理学, 助教 (20647101)
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| Research Collaborator |
Kajimura Ichige 東京慈恵会医科大学, 細胞生理学, 大学院生
Fujii Teruyuki 東京慈恵会医科大学, 麻酔科, 大学院生
Kuga Kazuhiro 東京慈恵会医科大学, 細胞生理学, 大学院生
Fujimoto Yoshitaka 東京慈恵会医科大学, 小児科, 大学院生
Kawachi Fumie 東京慈恵会医科大学, 小児科, 大学院生
Shimura Daisuke 早稲田大学, 先進理工学研究科, 大学院生
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥17,030,000 (Direct Cost: ¥13,100,000、Indirect Cost: ¥3,930,000)
Fiscal Year 2016: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2015: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥9,750,000 (Direct Cost: ¥7,500,000、Indirect Cost: ¥2,250,000)
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| Keywords | 未熟児 / 新生児 / 先天性心疾患 / vascular remodeling / プロスタグランジン / 血管内皮細胞 / 弾性線維 / 周産期ストレス / 絨毛膜炎 / 胎内感染 / 発達心血管学 / 新生児医療 / 血管分化 / 細胞外基質 / 酸素化 |
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| Outline of Final Research Achievements |
The ductus arteriosus (DA) is essential for fetal circulation and closes immediately after birth. It is very important to investigate the molecular mechanism of DA closure. In addition to the well-known vasodilatory role of PGE2, we previously found that PGE2-EP4 signal plays a critical role in charactering the DA structure. In the present study, we found that 1) NFkB inhibition promoted DA closure, 2) Oxygenation in blood after birth promoted intimal cushion formation and decreased secretion of elastin from DA smooth muscle cells, 3）Thromboxane A2 promoted DA closure, ４）Lipopolysaccharide delays closure of the rat DA by induction of inducible nitric oxide synthase but not prostaglandin E2. Our studies emphasize that a better understanding of DA vascular remodeling could encourage the design and development of novel pharmacological treatments for patients with patent DA or DA-dependent congenital heart diseases.
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