INTRODUCTION: The homeostasis of maternal-fetal fluid exchange is critically important in pregnancy. We sought to investigate the function of aquaporin 1 (AQP1) during pregnancy by examining fluid compartments of AQP1 knockout (AQP1-KO) mice. METHODS: Homozygous pregnant AQP1 knockout (KO) mice and control pregnant wild type CD1 mice were sacrificed. Placenta and fetal membranes were examined by immunohistochemical staining for expression of AQP1. The total number of embryos, atrophic embryos, and fetal and placental weight was recorded in each subgroup. Amniotic fluid amount in each sac was measured and amniotic fluid composition was determined. Analysis of variance of factorial design and one-factor analysis of variance were used for statistics. RESULTS: Immunohistochemistry performed on CD1, though not AQP1-KO, placenta revealed that AQP1 was expressed at the vascular endothelial cell, trophocyte, and amnion epithelial cell. In AQP1-KOs, the number of embryos decreased with advancing gestational age. Although the fetal weight of AQP1-KO mice was significantly lower than wild type, amniotic fluid amount was increased in AQP1-KO mice. The AQP1-KO placenta demonstrated increased degeneration with evidence of altered blood vessel structure and increased syncytiotrophoblast nodules. CONCLUSIONS: These findings demonstrate a critical role of AQP1 in placental and fetal growth and maternal-fetal fluid homeostasis.
INTRODUCTION: The homeostasis of maternal-fetal fluid exchange is critically important in pregnancy. We sought to investigate the function of aquaporin 1 (AQP1) during pregnancy by examining fluid compartments of AQP1 knockout (AQP1-KO) mice. METHODS: Homozygous pregnant AQP1 knockout (KO) mice and control pregnant wild type CD1mice were sacrificed. Placenta and fetal membranes were examined by immunohistochemical staining for expression of AQP1. The total number of embryos, atrophic embryos, and fetal and placental weight was recorded in each subgroup. Amniotic fluid amount in each sac was measured and amniotic fluid composition was determined. Analysis of variance of factorial design and one-factor analysis of variance were used for statistics. RESULTS: Immunohistochemistry performed on CD1, though not AQP1-KO, placenta revealed that AQP1 was expressed at the vascular endothelial cell, trophocyte, and amnion epithelial cell. In AQP1-KOs, the number of embryos decreased with advancing gestational age. Although the fetal weight of AQP1-KO mice was significantly lower than wild type, amniotic fluid amount was increased in AQP1-KO mice. The AQP1-KO placenta demonstrated increased degeneration with evidence of altered blood vessel structure and increased syncytiotrophoblast nodules. CONCLUSIONS: These findings demonstrate a critical role of AQP1 in placental and fetal growth and maternal-fetal fluid homeostasis.