A novel model of polyhydramnios: amniotic fluid volume is increased in aquaporin 1 knockout mice

• DOI: 10.1016/j.ajog.2005.02.046
• Publication Date: 2005-06-20T20:04:21Z
• Authors: Stephanie E. Mann; Emily A. Ricke; Elvina A. Torres; Robert N. Taylor
• Keywords: Polyhydramnios; Amnion; Knockout mouse; Gene knockout; Aquaporin 3; Fetal membrane

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.