| Project/Area Number |
15K19656
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 子宮内発育遅延 / Nod1 / 自然免疫 / 血管病変 / 胎児子宮内発育遅延 / 胎児発育遅延 |
|---|
| Outline of Final Research Achievements |
Nod1 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 about the deleterious effects of activated Nod1 signaling on embryonic growth and development. In this study, we demonstrated that administration of Nod1 ligand to pregnant mice induced IUGR and IUFD. Maternal injection of Nod1 ligand induced robust increases in the amounts of CCL2, IL-6, and TNF proteins as well as NO in maternal, placental and fetal tissues. CCL2 and IL-6 mRNAs were significantly induced in the fetal vascular tissues with maternal injection of Nod1 ligand than those in other tissues. Using Nod1-knockout mice, we verified that maternal Nod1 ligand directly induced upregulation of genes associated with immune response, inflammation, and apoptosis in fetal vascular tissues. Our data thus provided new evidence for the pathogenic role of Nod1 in the development of IUGR and IUFD at the maternal-fetal interface.
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