An In Vitro Model for Studying Interactions Between Mouse Trophoblast and Uterine Epithelial Cells

Morris, John E.; Potter, Sandra W.

doi:10.1007/978-1-4613-0615-3_3

Cited by 13 publications

(4 citation statements)

References 38 publications

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“…Implantation of the early embryo in the uterus requires that the uterus reaches the receptive stage and the trophoblast reaches the invasive stage synchronously. Uterine receptivity represents a change and/or loss in the expression of general epithelial phenotype of uterine epithelial cells [1–3] and is marked by reduced thickness of glycocalyx of uterine epithelial cells, changes in cell surfaces [4–6] and the biosynthesis and expression of new cell surface proteins [7–10]. The endometrial receptivity is maintained only for a limited time period defined as the implantation window and is regulated by estrogen and progesterone [11].…”

Section: Introductionmentioning

confidence: 99%

Profiling of E‐cadherin, β‐catenin and Ca²⁺ in embryo–uterine interactions at implantation

et al. 2006

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Establishment of early pregnancy is promoted by a complex network of signalling molecules that mediate cell-to-cell and cell-to-extracellular matrix communications between the receptive endometrium and the invasive trophectoderm. In this study, we have attempted to evaluate the expression profiles of cadherin and catenin during embryo implantation in the mouse. Western blotting studies along with immunocytochemical analysis revealed that E-cadherin is expressed rather ubiquitously in the uterine epithelial cells, distinct enrichment is observed on the apical membrane in the endometrium of peri-implantation uterus specifically at the implantation sites and not at the inter-implanation sites. b-Catenin also is upregulated and is specifically restricted to apical membrane of epithelial cells of implantation sites. Progesterone induced expression of E-cadherin and 17b-estradiol regulated the expression of catenin in implantation-delayed uteri. Interestingly, estradiol imparted negative modulation on cadherin expression when co-administered with progesterone. On the contrary, trophoblast exhibits a striking down regulation of cadherin, catenin and Ca 2+ at peri implanting stage. These observations suggest that the trophoblasts exhibited an invasive phenotype while the endometrial epithelium displayed an adhesive phenotype during the window of implantation. Thus, embryo implantation presents an instance where two interacting surfaces showed mutually complementing interaction phenotypes.

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Section: Introductionmentioning

confidence: 99%

Profiling of E‐cadherin, β‐catenin and Ca²⁺ in embryo–uterine interactions at implantation

et al. 2006

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“…o 1993 WiIry-Llss, inc. Embryo implantation is initiated by the adhesion of the apical plasma membrane of trophectodermal cells of the blastocyst to the apical plasma membrane of the uterine epithelium. The apical surface of the uterine epithelium is usually non-receptive to embryo attachment and becomes receptive only after appropriate hormonal stimulation (Denker, 1990;Morris and Potter, 1990). The implantation process also resembles invasion of malignant tumors and neovascularization (Denker, 1990) and so studies of a n implantation-related event may yield insight into other tissue invasion processes.…”

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Heparin‐like glycosaminoglycans participate in binding of a human trophoblastic cell line (JAR) to a human uterine epithelial cell line (RL95)

Rohde

Carson

1993

Journal Cellular Physiology

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In vitro studies in our laboratory have indicated that heparan sulfate proteoglycans (HSPGs) play an important role in murine embryo implantation. In order to investigate the potential function of HSPGs in human implantation, two human cell lines (RL95 and JAR) were used to model uterine epithelium and embryonal trophectoderm, respectively. A heterologous cell-cell adhesion assay was developed to determine if binding of JAR cells to RL95 cells was heparan sulfate-dependent. Labeled, single cell suspensions of JAR cells attached to confluent monolayers of RL95 cells in a dose- and time-dependent manner. Heparin-like glycosaminoglycans and JAR cell proteoglycans competitively inhibited JAR cell adhesion to RL95 cells by 50% or more. A panel of chemically modified heparins were used to demonstrate that O-sulfation and amino group substitution were critical for inhibition of cell-cell adhesion. Treatment with chlorate, an inhibitor of ATP-sulfurylase, resulted in a 56% reduction in cell-cell binding compared to untreated controls. Heparinase and chondroitinase ABC markedly inhibited JAR-RL95 binding, while chondroitinase AC had no significant effect. These observations indicated that HSPGs as well as dermatan sulfate-containing proteoglycans participated in cell-cell binding. Collectively, these results indicate that initial binding interactions between JAR and RL95 cells is mediated by cell surface glycosaminoglycans (GAGs) with heparin-like properties (i.e., heparan sulfate and dermatan sulfate). These observations are consistent with an important role for HS and heparin-like GAGs as well as their corresponding binding sites in early stages of human trophoblast-uterine epithelial cell binding.

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“…a reduction in the thickness of the glycocalyx of uterine epithelial cells and in cell surface charge [Enders and Schlafke, 1977;Anderson et al, 1990;Morris and Potter, 1990;Carson et al, 1998a, b;Aplin, 1999;Niklaus et al, 2001] and/or the biosynthesis and expression of new cell surface proteins as well as of cell surface-bound glycoconjugates [Lampelo et al, 1985;Anderson et al, 1988;Kimber and Lindenberg, 1990;Hoffman et al, 1996;Carson et al, 1998b;Olson et al, 1998;Illingworth and Kimber, 1999;Niklaus et al, 1999]. However, a number of findings suggest that much more than the expression of apical membrane-associated molecules is changed in the uterine epithelium at acquisition of receptivity, i.e.…”

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In vitro Studies on Endometrial Adhesiveness for Trophoblast: Cellular Dynamics in Uterine Epithelial Cells

Thie

Denker

2002

Cells Tissues Organs

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Initiation of embryo implantation involves adhesion of trophoblast cells to the epithelial lining of the endometrium. The mechanisms regulating the adhesive properties of the uterine epithelium for trophoblast during initiation of human embryo implantation, however, are still incompletely understood. We report here on model studies that we have performed in our laboratory, and in particular on certain methodological approaches that seem to yield new insight into basic mechanisms involved. Of central interest is the ability of the uterine epithelium to develop an adhesion competence at its apical cell pole. This confronts us with a cell biological paradox in that adhesion must be established at the pole which in simple epithelia is typically specialized to resist adhesion. Gain of apical adhesion competence by uterine epithelial cells should be related to cellular rearrangements, i.e. a modulation of their apicobasal cell polarity. Here, we used monolayer-cultured uterine epithelial RL95-2 cells as an in vitro model for the human receptive uterine epithelium. We demonstrated that formation of stable cell-to-cell bonds between the free (apical) pole of these cells and attaching trophoblast (modelled by JAr cells) depends on a number of structural and functional peculiarities that RL95-2 cells have in contrast to other uterine epithelial cells (HEC-1-A cells) which resist attachment via this cell pole. RL95-2 cells were shown to lack tight junctions and to exhibit only rudimentary adherens junctions and a non-polar organization of the actin cytoskeleton. Using the atomic force microscope in a force spectroscopy mode, we exactly defined the time dependence of adhesive interactions between RL95-2 cells and trophoblast, measured the pressure force needed to initiate this process, and screened the buildup of the adhesive forces between the binding partners. A dynamic interaction between the actin cytoskeleton and integrins (a prerequisite for functional activity of integrins) was shown to be an important aspect of the adhesive properties of RL95-2 cells. In addition, at least two types of calcium channels in the plasma membrane of RL95-2 cells seem to play a role in activation of a variety of calcium-sensitive response mechanisms including adhesiveness for trophoblast, i.e. diltiazem-sensitive channels seem to contribute to the initiation of JAr cell binding and SKF-96365-sensitive channels to participate in a feedback loop that controls the balance of bonds. By extrapolation, these data suggest an active role of the uterine epithelium in the process of embryo implantation which we are just beginning to understand in terms of its cell biology.

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An In Vitro Model for Studying Interactions Between Mouse Trophoblast and Uterine Epithelial Cells

Cited by 13 publications

References 38 publications

Profiling of E‐cadherin, β‐catenin and Ca²⁺ in embryo–uterine interactions at implantation

Profiling of E‐cadherin, β‐catenin and Ca²⁺ in embryo–uterine interactions at implantation

Heparin‐like glycosaminoglycans participate in binding of a human trophoblastic cell line (JAR) to a human uterine epithelial cell line (RL95)

In vitro Studies on Endometrial Adhesiveness for Trophoblast: Cellular Dynamics in Uterine Epithelial Cells

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An In Vitro Model for Studying Interactions Between Mouse Trophoblast and Uterine Epithelial Cells

Cited by 13 publications

References 38 publications

Profiling of E‐cadherin, β‐catenin and Ca2+ in embryo–uterine interactions at implantation

Profiling of E‐cadherin, β‐catenin and Ca2+ in embryo–uterine interactions at implantation

Heparin‐like glycosaminoglycans participate in binding of a human trophoblastic cell line (JAR) to a human uterine epithelial cell line (RL95)

In vitro Studies on Endometrial Adhesiveness for Trophoblast: Cellular Dynamics in Uterine Epithelial Cells

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Profiling of E‐cadherin, β‐catenin and Ca²⁺ in embryo–uterine interactions at implantation

Profiling of E‐cadherin, β‐catenin and Ca²⁺ in embryo–uterine interactions at implantation