| Project/Area Number |
24659509
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
HARA TOSHIRO 九州大学, 医学(系)研究科(研究院), 教授 (40150445)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIO Hisanori 九州大学, 大学病院, 助教 (00507783)
NAGATA Hazumu 九州大学, 医学(系)研究科(研究院), 助教 (20570790)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 自然免疫 / 子宮内胎児発育遅延 / 子宮内胎児死亡 / Nod1 / 周産期 / 子宮内発育遅延 / 自然免疫受容体 / NOD1 |
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| Research Abstract |
Nod1 (nucleotide-binding oligomerization domain containing 1) is one of the pattern recognition receptors that play an important role in the induction of innate immune and inflammatory responses. However, little is known regarding the effects of direct activation of Nod1 on fetus or newborn. In this study, we demonstrated that administration of Nod1 ligand to pregnant mice induced intrauterine fetal death and growth restriction. We also found that fetuses were affected by transplacental passage of maternal Nod1 ligand. We examined the role of Nod1 signaling in a fetal mouse with a focus on the development of vasculopathy. Our observation suggests a possible link between Nod1 ligands-mediated activation of the innate immune system in fetus and IUGR and might offer a new strategy to improve the long-term cardiovascular health of IUGR cases.
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