Mann Stephanie E, Ricke Emily A, Torres Elvina A, Taylor Robert N
Department of Obstetrics, Gynecology, and Reproductive Sciences and Medicine, University of California, San Francisco, USA.
Am J Obstet Gynecol. 2005 Jun;192(6):2041-4; discussion 2044-6. doi: 10.1016/j.ajog.2005.02.046.
To test the hypothesis that amniotic fluid volume is increased in aquaporin 1 knockout mice.
Transgenic mice deficient in aquaporin 1 protein were generated by targeted gene disruption, as described previously. After a cesarean section was performed, intact, individual gestational sacs were removed from the uterus and weighed. Amniotic fluid volume, osmolality, and fetal and placental weights were determined. Data were analyzed by a 1-way analysis of variance for ranks; Dunn's post hoc test was used to analyze significant trends.
Analysis of 16 litters showed 35 wild-type, 52 heterozygote, and 33 aquaporin 1 knockout mice. The knockout mice had a greater volume of amniotic fluid and lower amniotic fluid osmolality than their wild-type and heterozygote counterparts. There were no significant differences in fetal or placental weights among the groups.
Aquaporin 1 null fetuses produce a greater volume of more dilute amniotic fluid. Our findings show that aquaporin 1 water channels in fetal membranes may contribute to amniotic fluid volume regulation. We speculate that idiopathic polyhydramnios may be associated with a deficiency of aquaporin 1 channels in human fetal membranes. Transgenic aquaporin 1 knockout mice provide a unique animal of polyhydramnios.
验证水通道蛋白1基因敲除小鼠羊水量增加这一假说。
如前所述，通过靶向基因敲除构建水通道蛋白1蛋白缺陷型转基因小鼠。剖宫产术后，从子宫中取出完整的单个妊娠囊并称重。测定羊水量、渗透压以及胎儿和胎盘重量。数据采用单向秩和方差分析进行分析；Dunn事后检验用于分析显著趋势。
对16窝小鼠的分析显示，有35只野生型、52只杂合子和33只水通道蛋白1基因敲除小鼠。与野生型和杂合子小鼠相比，基因敲除小鼠的羊水量更多，羊水渗透压更低。各组间胎儿或胎盘重量无显著差异。
水通道蛋白1基因缺失的胎儿产生的羊水更多且更稀。我们的研究结果表明，胎膜中的水通道蛋白1水通道可能有助于羊水容量的调节。我们推测，特发性羊水过多可能与人胎膜中水通道蛋白1通道缺乏有关。转基因水通道蛋白1基因敲除小鼠为羊水过多提供了一种独特的动物模型。
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