Pregnant phenotype in aquaporin 8-deficient mice
Pregnant phenotype in aquaporin 8-deficient mice
复制标题
水通道蛋白8缺陷小鼠的妊娠表型
DOI：
10.1038/aps.2011.45
复制
发表时间：
2011-06-01
影响因子：
8.2
通讯作者：
Ma, Tong-hui
中科院分区：
文献类型：
--
作者：
Sha, Xiao-yan;Xiong, Zheng-fang;Ma, Tong-hui
目的：水通道蛋白8（AQP8）在女性生殖系统中表达，但其生理功能仍需阐明。本研究利用AQP8敲除(AQP8-KO)小鼠探讨AQP8在妊娠过程中的作用。方法：将纯合子AQP8-KO小鼠交配，记录受孕率。 AQP8-KO妊娠小鼠或其子代根据胎儿孕日(7、13、16、18GD)和新生儿分为5个亚组。野生型C57怀孕小鼠作为对照组。记录每个亚组的怀孕小鼠、胚胎总数和萎缩胚胎的数量，以及胎儿重量、胎盘重量和胎盘面积。计算 13、16 和 18 GD 时每个囊中的羊水量。通过因子设计方差分析和卡方检验确定统计学显着性。结果：AQP8-KO和野生型小鼠的受孕率没有显着差异。与野生型对照相比，AQP8-KO 怀孕小鼠的胚胎数量显着增加。与年龄匹配的野生型对照相比，AQP8-KO 组的胎儿/新生儿体重也显着更大。尽管 FM/AFA（胎儿体重/羊水量）没有差异，但 AQP8-KO 怀孕小鼠的羊水量高于野生型对照小鼠。虽然 AQP8-KO 胎盘重量显着大于野生型对照，但两组均没有胎盘病理学证据。结论：结果表明 AQP8 缺陷在妊娠结局中发挥重要作用。简介水通道蛋白 (AQP) 构成了一个不断增长的水特异性膜通道蛋白家族，可跨细胞膜运输水 1, 2。目前已知有 13 种哺乳动物水通道蛋白 (AQP0-12)；这些分子的一部分能够增加小分子的渗透性，例如甘油 (AQP3, 7, 9) 和尿素 (AQP3, 7, 8, 9)。据报道，AQP8 可渗透氨 3。大多数水通道蛋白在质膜中组成型表达 (AQP0, 1, 3, 4, 7, 8, 9, 10)，而其他水通道蛋白几乎完全局限于细胞内膜 (AQP6, 11, 12) 4。
Aim:Aquaporin 8 (AQP8) is expressed within the female reproductive system but its physiological function reminds to be elucidated. This study investigates the role of AQP8 during pregnancy using AQP8-knockout (AQP8-KO) mice.Methods:Homozygous AQP8-KO mice were mated, and the conception rate was recorded. AQP8-KO pregnant mice or their offspring were divided into 5 subgroups according to fetal gestational day (7, 13, 16, 18 GD) and newborn. Wild type C57 pregnant mice served as the control group. The number of pregnant mice, total embryos and atrophic embryos, as well as fetal weight, placental weight and placental area were recorded for each subgroup. The amount of amniotic fluid in each sac at 13, 16, and 18 GD was calculated. Statistical significance was determined by analysis of variance of factorial design and chi-square tests.Results:Conception rates did not differ significantly between AQP8-KO and wild type mice. AQP8-KO pregnant mice had a significantly higher number of embryos compared to wild type controls. Fetal/neonatal weight was also significantly greater in the AQP8-KO group compared to age-matched wild type controls. The amount of amniotic fluid was greater in AQP8-KO pregnant mice than wild type controls, although the FM/AFA (fetal weight/amniotic fluid amount) did not differ. While AQP8-KO placental weight was significantly larger than wild type controls, there was no evidence of placental pathology in either group.Conclusion:The results suggest that AQP8 deficiency plays an important role in pregnancy outcome.IntroductionAquaporins (AQPs) constitute a growing family of water-specific membrane channel proteins that transport water across cell membranes 1, 2. There are currently 13 known mammalian aquaporins (AQP0-12); a subset of these molecules are capable of increasing the permeability of small molecules such as glycerol (AQP3, 7, 9) and urea (AQP3, 7, 8, 9). AQP8 is reportedly permeable to ammonia 3. The majority of aquaporins are constitutively expressed in the plasma membrane (AQP0, 1, 3, 4, 7, 8, 9, 10), while others are almost exclusively restricted to intracellular membranes (AQP6, 11, 12) 4.