Placental and Membrane Aquaporin Water Channels: Correlation with Amniotic Fluid Volume and Composition

Beall, Marie H.; Wang, S.; Yang, Baoxue; Chaudhri, Nimra; Amidi, Fataneh; Ross, Michael G.

doi:10.1016/j.placenta.2006.06.005

Cited by 66 publications

(40 citation statements)

References 30 publications

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“…Transcriptomic analysis of a pregnant uterus of the C. ocellatus skink revealed significant upregulation of multiple members of the aquaporin gene family, including AQ3, AQ5, and AQ11 . In contrast, the primary aquaporins involved in placental water transport in mammals are AQ3, AQ8, and AQ9 (Wang et al 2001, Beall et al 2007. Future transcriptomic analyses of oviparous species will reveal whether the upregulation of aquaporins is specific to viviparous species, but functional studies are also needed to determine the functions of each aquaporin.…”

Section: Water Transportmentioning

confidence: 99%

The evolution of viviparity: molecular and genomic data from squamate reptiles advance understanding of live birth in amniotes

2014

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Squamate reptiles (lizards and snakes) are an ideal model system for testing hypotheses regarding the evolution of viviparity (live birth) in amniote vertebrates. Viviparity has evolved over 100 times in squamates, resulting in major changes in reproductive physiology. At a minimum, all viviparous squamates exhibit placentae formed by the appositions of maternal and embryonic tissues, which are homologous in origin with the tissues that form the placenta in therian mammals. These placentae facilitate adhesion of the conceptus to the uterus as well as exchange of oxygen, carbon dioxide, water, sodium, and calcium. However, most viviparous squamates continue to rely on yolk for nearly all of their organic nutrition. In contrast, some species, which rely on the placenta for at least a portion of organic nutrition, exhibit complex placental specializations associated with the transport of amino acids and fatty acids. Some viviparous squamates also exhibit reduced immunocompetence during pregnancy, which could be the result of immunosuppression to protect developing embryos. Recent molecular studies using both candidate-gene and next-generation sequencing approaches have suggested that at least some of the genes and gene families underlying these phenomena play similar roles in the uterus and placenta of viviparous mammals and squamates. Therefore, studies of the evolution of viviparity in squamates should inform hypotheses of the evolution of viviparity in all amniotes, including mammals.Reproduction (2014) 147 R15-R26

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Section: Water Transportmentioning

confidence: 99%

The evolution of viviparity: molecular and genomic data from squamate reptiles advance understanding of live birth in amniotes

2014

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“…Comparison of the pregnant phenotype of AQP8-deficient mice with that of wild type controls revealed elevations in embryo number, fetus/newborn weight (16 GD, 18 GD, and newborn), and the amount of amniotic fluid at each gestational age. While a broad tissue distribution of AQP8 has been reported in rat, mouse and human, strong expression has been reported within the female reproductive system, in particular in the placentas and fetal membranes of sheep, human and mouse and in the cervix of the mouse [16][17][18][19] . The reproductive impact of AQP8 deficiency has been addressed previously.…”

Section: Discussionmentioning

confidence: 99%

“…Subsequent studies [10][11][12][13][14][15][16] have shown that AQP8 has a wide tissue distribution in mammals, with expression noted in the testis, kidney, heart, gastrointestinal tract, airway, salivary gland, pancreas and placenta. In the reproductive system, AQP8 is strongly expressed in the testis and sperm in the male and in the ovary, oviduct, uterus, placenta, amnion, chorion and cervix in the female [16][17][18][19][20][21][22][23][24][25] . While an earlier study [26] of AQP8 null mice reported no significant differences in comparison to wild type controls with the exceptions of an increase in testicular volume and a reduction in water permeability within the testes, we observed that AQP8 deficiency increased the number of mature follicles and the resulting fertility of female mice [27] .…”

Section: Introductionmentioning

confidence: 99%

Pregnant phenotype in aquaporin 8-deficient mice

et al. 2011

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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.

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“…Indeed, the authors note that aquaporin 9 was the only member of its family identified in human fetal membranes via Northern analysis, supporting their hypothesis that this aquaglyceroporin is involved in integral mechanisms of amniotic fluid homeostasis. In support of this view, Beall et al [60] report a negative correlation between placental aquaporin 9 expression and amniotic fluid volume in a mouse model; (2) a compelling body of evidence supports the concept that regulation of uterine luminal fluid is necessary for successful blastocyst implantation. Both surface epithelial cells and glandular epithelium have been implicated in this process, in which aquaporins have been shown to play a role.…”

Section: Normal Pregnancy and Aquaporinmentioning

confidence: 94%

Fetal membranes as an interface between inflammation and metabolism: Increased Aquaporin 9 expression in the presence of spontaneous labor at term and chorioamnionitis

Mittal¹,

Romero²,

Mazaki‐Tovi³

et al. 2009

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective. Aquaporin 9 (AQP9) is a water channel protein characterized by its high permeability to nutrients such as lactate and glycerol, as well as urea and other small solutes. These unique properties of AQP9 suggest that this molecule may play a role in the modulation of nutrient flux through the fetal membranes in conditions associated with increased metabolic demand, such as spontaneous labor and inflammation. The objective of this study was to determine the expression of AQP9 in the chorioamniotic membranes from women with and without term labor, as well as those with preterm prelabor rupture of membranes (PPROM) with and without histologic chorioamnionitis. Study design. A cross-sectional study was performed which included patients in the following groups: (1) term not in labor (TNL; n ¼ 14); (2) term, spontaneous labor (n ¼ 14); and (3) PPROM with (n ¼ 20) and without (n ¼ 17) histologic chorioamnionitis. AQP9 mRNA expression in fetal membranes was quantified using quantitative real-time reverse transcription-polymerase chain reaction and analyzed with a linear model including gestational age as a covariate. Results. (1) AQP9 mRNA expression was identified in all chorioamniotic membrane specimens; (2) AQP9 expression in fetal membranes was significantly higher in spontaneous term labor when compared with TNL (fold change 3.6; p ¼ 0.01); and (3) Among patients with PPROM, the presence of histologic chorioamnionitis was associated with a higher expression of AQP9 in the chorioamniotic membranes compared with those from women without histologic chorioamnionitis (fold change 8.7; p 5 0.001). Conclusion. Aquaporin 9 mRNA expression is higher in the fetal membranes from patients with spontaneous term labor and those with PPROM and histologic chorioamnionitis. These findings are novel, and suggest a role for aquaporin 9 in membrane-mediated transfer of nutrients to support the increased metabolic demands associated with the host immune response of the terminal pathway of parturition and histologic chorioamnionitis.

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Placental and Membrane Aquaporin Water Channels: Correlation with Amniotic Fluid Volume and Composition

Cited by 66 publications

References 30 publications

The evolution of viviparity: molecular and genomic data from squamate reptiles advance understanding of live birth in amniotes

The evolution of viviparity: molecular and genomic data from squamate reptiles advance understanding of live birth in amniotes

Pregnant phenotype in aquaporin 8-deficient mice

Fetal membranes as an interface between inflammation and metabolism: Increased Aquaporin 9 expression in the presence of spontaneous labor at term and chorioamnionitis

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