2013 Fiscal Year Final Research Report
Molecular mechanisms of ductus arteriosus closure
| Project/Area Number |
23390277
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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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 (2012-2013)
Waseda University (2011) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YOKOYAMA Utako 横浜市立大学, 医学部, 講師 (70404994)
GODA Nobuhito 早稲田大学, 理工学術院, 教授 (00245549)
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| Co-Investigator(Renkei-kenkyūsha) |
ISHIKAWA Yoshihiro 横浜市立大学, 横浜市立大学, 教授 (40305470)
NAKAMURA Tomoyuki 関西医科大学, 医学部, 教授 (20362527)
SUGIMOTO Yukihiko 熊本大学, 生命科学研究部, 教授 (80243038)
AOKI Hiroki 久留米大学, 循環器病研究所, 教授 (60322244)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Keywords | vascular remodeling / 動脈管 / 新生児 / 弾性線維 / プロスタグランジン / 酸素化 |
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| Research Abstract |
The ductus arteriosus (DA) is an essential fetal artery that closes immediately after birth. However, the molecular mechanisms remain unknown, especially its vascular remodeling. We found that 1) prostaglandin E2 (PGE2) -EP4 signaling decreased elastic fiber formation through degradation of the cross-linking enzyme lysyl oxidase, and that 2) NFkB signal could be activated by PGE2-EP4 stimulation via cAMP-independent pathway, and that 3) endothelial cells of the DA exhibited a unique gene profile involved in the regulation of DA-specific morphology and function. These novel findings regarding DA vascular remodeling could open a possibility to innovate a new therapeutic strategy for the regulation of DA closure.
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