Endoplasmic reticulum stress-induced fetal growth retardation is associated with placental dysfunction

内质网应激引起的胎儿生长迟缓与胎盘功能障碍有关

• 批准号: 22790551
• 负责人: KAWAKAMI Takashige
• 金额: $ 2.5万
• 依托单位: Tokushima Bunri University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22790551/
• 关键词: 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; 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

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.

为了研究内质网（ER）应激对占位术功能和胎儿生长的影响，每天用20、40和60μg/kg/kg/天的剂量对孕妇（TUN）注射孕妇（TUN）从妊娠日（GD）12.5到GD16.5.tun治疗的剂量增加了plosenta和Fetus的重量。此外，TUN处理增加了斑点SLC2A3/GLUT3 mRNA表达水平，这是主要的lopenal葡萄糖转运蛋白之一，而它改善了SLC2A1/GLUT1 mRNA表达水平。 4-苯基丁酸钠是一种化学伴侣，可预防小鼠内质网应激诱导的宫内宫内生长迟缓。这些结果表明，持续暴露于ER应力会破坏葡萄糖供应从大坝到胎儿的葡萄糖供应，至少部分部分，葡萄糖转运蛋白的表达变化会导致低出生体重。