| Project/Area Number |
16K19680
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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 | Chiba University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | オートファジー / インスリン様成長因子 / 成長障害 / 子宮内発育不全 |
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| Outline of Final Research Achievements |
TTo reveal the effect of autophagy on the fetal growth, we stimulated wild type (WT) and ATG5 knock-out (ATG5KO) mouse embryonic fibroblast (MEF) cells with serum-free stimulation only or serum-free and hypoxia stimulation. With serum-free stimulation, ATG5KO MEF cells showed increased AKT phosphorylation both before and after 10nM IGF-1 stimulation compared with WT MEF cells. We also found AKT phosphorylation in ATG5KO MEF cells was increased with serum-free and hypoxia stimulation compared with WT MEF cells. These data suggest that there might be a cross-talk between autophagy and insulin-like growth factor signaling. Next, we investigated the effect in vivo, using IUGR model mouse induced by thromboxane A2 analog. However, we did not see the difference between WT and ATG5KO mouse. Further studies would be required to verify the effect of autophagy on intrauterine growth retardation.
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