Morphologic effects of epithelial ion channels on the mouse uterus: differences between raloxifene analog (LY117018) and estradiol treatments

Nobuzane, Takahiro; Tashiro, Satoshi; Kudo, Yoshiki

doi:10.1016/j.ajog.2008.03.047

Cited by 11 publications

(8 citation statements)

References 26 publications

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“…Previous studies demonstrate that ENaC is primarily localized to the apical membrane of both luminal and glandular epithelia, while CFTR is predominantly expressed in the stromal cells (Chan et al, 2002; Ruan et al, 2012; Yang et al, 2004). Estrogen induces CFTR expression, but represses ENaC, resulting in fluid accumulation in the uterine lumen, whereas progesterone acts oppositely in regulating these two genes for fluid reabsorption in the uterus (Nobuzane et al, 2008; Zheng et al, 2004). Abnormal uterine fluid accumulation and implantation failure have also been observed when CFTR expression is aberrantly upregulated by inflammation in mice (He et al, 2010).…”

Section: Cell-cell Interactions: the Nature Of Embryo Implantationmentioning

confidence: 99%

Physiological and molecular determinants of embryo implantation

Zhang

Lin

Kong

et al. 2013

Molecular Aspects of Medicine

450

480

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Embryo implantation involves the intimate interaction between an implantation-competent blastocyst and a receptive uterus, which occurs in a limited time period known as the window of implantation. Emerging evidence shows that defects originating during embryo implantation induce ripple effects with adverse consequences on later gestation events, highlighting the significance of this event for pregnancy success. Although a multitude of cellular events and molecular pathways involved in embryo-uterine crosstalk during implantation have been identified through gene expression studies and genetically engineered mouse models, a comprehensive understanding of the nature of embryo implantation is still missing. This review focuses on recent progress with particular attention to physiological and molecular determinants of blastocyst activation, uterine receptivity, blastocyst attachment and uterine decidualization. A better understanding of underlying mechanisms governing embryo implantation should generate new strategies to rectify implantation failure and improve pregnancy rates in women.

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Section: Cell-cell Interactions: the Nature Of Embryo Implantationmentioning

confidence: 99%

Physiological and molecular determinants of embryo implantation

Zhang

Lin

Kong

et al. 2013

Molecular Aspects of Medicine

450

480

View full text Add to dashboard Cite

show abstract

“…Aberrant upregulation of CFTR or inhibition of uterine ENaC leads to abnormal uterine fluid accumulation and implantation failure. Progesterone has been shown to repress the expression of CFTR while stimulating uterine ENaC induction, which is condu- cive to embryo implantation (Nobuzane et al, 2008, Zheng et al, 2004. Moreover, it has been shown that serum and glucocorticoid inducible kinase-1 (SGK1), a key regulator of sodium transport in mammalian epithelia (Fejes-Toth et al, 2008), can enhance ENaC expression via inhibiting the ubiquitin ligase, neural precursor cell expressed developmentally down-regulated protein (NEDD) 4-2 (Lang et al, 2006).…”

Section: Luminal Closurementioning

confidence: 99%

Molecular determinants of uterine receptivity

Tu¹,

Hao²,

Zhang³

et al. 2014

Int. J. Dev. Biol.

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Uterine receptivity is defined as a limited period when the uterine environment is conducive to blastocyst acceptance and implantation. Any disturbance of this early pregnancy event will compromise pregnancy success. In this review, we first briefly summarize uterine morphological coordination for the attainment of receptivity, then focus on elucidating the molecular complexity in establishing uterine receptivity and hence embryo implantation. A better understanding of the molecular basis governing uterine receptivity will help to improve the outcome of natural pregnancy and pregnancy conceived via assisted reproductive techniques.

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“…For example, interplay between the cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial sodium channel (ENaC), as well as potassium (K 1 ) channels, are vital in regulating uterine electrolyte and fluid transport. This is very important in terms of reducing the volume of uterine luminal fluid, in order to lock the embryo in place prior to implantation (Nobuzane et al, 2008). ENaC also senses mechanical and chemical signals from the embryo and transduces downstream cellular responses to promote stromal decidualization (Enuka et al, 2012;Ruan et al, 2014).…”

Section: Ion Channelsmentioning

confidence: 99%

Molecular mechanisms of membrane interaction at implantation

Davidson

Coward

2016

Birth Defects Research Pt C

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Successful pregnancy is dependent upon the implantation of a competent embryo into a receptive endometrium. Despite major advancement in our understanding of reproductive medicine over the last few decades, implantation failure still occurs in both normal pregnancies and those created artificially by assisted reproductive technology (ART). Consequently, there is significant interest in elucidating the etiology of implantation failure. The complex multistep process of implantation begins when the developing embryo first makes contact with the plasma membrane of epithelial cells within the uterine environment. However, although this biological interaction marks the beginning of a fundamental developmental process, our knowledge of the intricate physiological and molecular processes involved remains sparse. In this synopsis, we aim to provide an overview of our current understanding of the morphological changes which occur to the plasma membrane of the uterine endothelium, and the molecular mechanisms that control communication between the early embryo and the endometrium during implantation. A multitude of molecular factors have been implicated in this complex process, including endometrial integrins, extracellular matrix molecules, adhesion molecules, growth factors, and ion channels. We also explore the development of in vitro models for embryo implantation to help researchers investigate mechanisms which may underlie implantation failure. Understanding the precise molecular pathways associated with implantation failure could help us to generate new prognostic/diagnostic biomarkers, and may identify novel therapeutic targets.

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Morphologic effects of epithelial ion channels on the mouse uterus: differences between raloxifene analog (LY117018) and estradiol treatments

Abstract: Estradiol and LY117018 differentially regulate the expression of CFTR and ENaC in ovariectomized mouse uterus. This finding suggests that uterine fluid accumulation can be controlled mainly by targeting the ENaC.

Cited by 11 publications

References 26 publications

Physiological and molecular determinants of embryo implantation

Physiological and molecular determinants of embryo implantation

Molecular determinants of uterine receptivity

Molecular mechanisms of membrane interaction at implantation

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