Abstract

To explore the effects of aquaporin (AQP) 1 on pregnancy outcome and the association between expression of AQP1 and other AQPs in the placenta and foetal membranes, the rate of copulatory plugs and pregnancy, amniotic fluid (AF) volume, osmolality and composition were determined in AQP1-knockout (AQP1−/−) mice at different gestational days (GD). The expression and location of AQP1 and other AQPs in the placenta and foetal membranes of AQP1−/− mice, AQP1-siRNA transfected WISH cells and oligohydramnios patients were also detected. Compared to control mice, AQP1−/− mice exhibited reduced copulation plug and successful pregnancy rates, but these effects were accompanied by a larger AF volume and lower AF osmolality at late gestation. AQP9 expression was significantly decreased in the placenta and foetal membranes of AQP1−/− mice, while AQP8 level was elevated in the foetal membranes of AQP1−/− mice. Moreover, AQP9 expression was suppressed in WISH cells after AQP1 downregulation. Furthermore, AQP9 expression was associated with AQP1 level in the placenta and foetal membranes in oligohydramnios. AQP1 may play a critical role in regulating pregnancy outcome and maternal-foetal fluid homeostasis. Changes in AQP1 expression may lead to compensatory alterations in AQP8 and AQP9 expression in the placenta.

Highlights

  • The homeostasis of amniotic fluid (AF) exchange between matrix and foetus plays a vital role in a successful pregnancy, as either polyhydramnios or oligohydramnios may increase foetal morbidity and mortality during the perinatal stage (Ducza et al 2017)

  • We found that pregnant AQP1−/− mice exhibited a reduced copulation plug rate (50%, 30/60) compared with that in pregnant AQP1+/+ mice (90%, 54/60), suggesting that AQP1 depletion led to a decrease in the copulation plug rate (χ2 = 4.09, P = 0.043)

  • These results show that AQP1 deficiency reduces reproductive performance in female mice

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Summary

Introduction

The homeostasis of amniotic fluid (AF) exchange between matrix and foetus plays a vital role in a successful pregnancy, as either polyhydramnios (excess AF) or oligohydramnios (insufficient AF) may increase foetal morbidity and mortality during the perinatal stage (Ducza et al 2017). The underlying cellular and molecular mechanisms of solute and water transport between the foetal and maternal compartments remain elusive and require investigation. During the latter period of gestation, AF is mainly derived from foetal urine and a portion of the lung fluid (Brace and Cheung 2014). The authors did not observe the changes in AF volume and osmolality in mice with AQP1 depletion during different gestational days.

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