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首页> 外文期刊>Physiological Reports >Hypoxia reduces placental mTOR activation in a hypoxia‐induced model of intrauterine growth restriction (IUGR)
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Hypoxia reduces placental mTOR activation in a hypoxia‐induced model of intrauterine growth restriction (IUGR)

机译：缺氧可在缺氧引起的宫内生长受限（IUGR）模型中降低胎盘mTOR激活

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AbstractMammalian target of rapamycin (mTOR) is a protein that regulates cell growth in response to altered nutrient and growth factor availability. Our objective was to assess activated mTOR and its intracellular intermediates p70, and 4EBP1 in placental and invasive trophoblast cells in a hypoxia-induced model of intrauterine growth restriction (IUGR) in rats. Rats were treated with hypoxia (9%) for 4 days. Placental and fetal weights, as well as conceptus numbers were recorded at the time of necropsy. Immunohistochemistry was used to determine the level of trophoblast invasion and apoptosis. Western blots were used to determine the activation of mTOR, p70, and 4EBP1 in the placenta and the uterine mesometrial compartment. We observed (1) decreased placental (21%) and fetal (24%) weights (P  0.05); (2) decreased trophoblast invasion; (3) significantly increased active 4EBP1 (28%; P  0.05) in invasive trophoblast cells yet no changes in the activation of mTOR and p70 proteins; and (4) a significant decrease in the activation of mTOR (48%; P  0.05) with no differences in p70 or 4EBP1 activation in the placenta. We conclude that the development of IUGR is correlated with decreased activation of the mTOR protein in the placenta and increased 4EBP1 activity in the invading trophoblast. These results provide important insight into the physiological relevance of these pathways. Furthermore, modification of these and other related targets during gestation may alleviate IUGR severity.
机译：摘要哺乳动物雷帕霉素靶标（mTOR）是一种蛋白质，可调节细胞生长，以响应营养物和生长因子利用率的变化。我们的目的是在缺氧诱导的宫内生长受限（IUGR）模型中评估胎盘和浸润性滋养层细胞中活化的mTOR及其细胞内中间体p70和4EBP1。大鼠接受低氧（9％）治疗4天。剖检时记录胎盘和胎儿的重量，以及妊娠数。免疫组织化学用于确定滋养细胞侵袭和凋亡的水平。 Western印迹用于确定胎盘和子宫体间室中mTOR，p70和4EBP1的激活。我们观察到（1）胎盘重量（21％）和胎儿重量（24％）下降（P <0.05）; （2）滋养细胞浸润减少; （3）浸润性滋养层细胞中活性4EBP1显着增加（28％; P <0.05），但mTOR和p70蛋白的激活没有变化; （4）mTOR的激活显着降低（48％; P <0.05），胎盘中p70或4EBP1的激活没有差异。我们得出的结论是，IUGR的发展与胎盘中mTOR蛋白的激活减少以及侵袭性滋养细胞中4EBP1活性的增加有关。这些结果提供了对这些途径的生理相关性的重要见解。此外，在妊娠期间对这些及其他相关靶标的修饰可减轻IUGR的严重性。

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