Endoplasmic reticulum stress-induced fetal growth retardation is associated with placental dysfunction
| Project/Area Number |
22790551
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hygiene
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| Research Institution | Tokushima Bunri University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 小胞体ストレス / 胎盤 / 胎仔発育遅延 / グルコーストランスポーター / 胎児発育遅延 |
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| Research Abstract |
In order to investigate the effect of endoplasmic reticulum(ER) stress on placental function and fetal growth, the pregnant mice were treated with daily injections of tunicamycin(Tun) at doses of 20, 40, and 60μg/kg/day from gestation day(GD) 12.5 to GD16.5.Tun treatment decreased the weight of placenta and fetus. Furthermore, Tun treatment increased placental Slc2a3/GLUT3 mRNA expression level, which is one of the major placental glucose transporter, while it decreased the Slc2a1/GLUT1 mRNA expression level. Sodium 4-phenylbutyrate, a chemical chaperone, protects against endoplasmic reticulum stress-induced intrauterine growth retardation in mice. These results suggest that continuous exposure to ER stress disrupts glucose supply from dam to fetus via placenta, at least in part, with altered expressions of glucose transporters resulting in low birth weight.
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Report
(3 results)
Research Products
(21 results)
