Relationship between the Programs for Implantation and Trophoblast Differentiation

Sherman, Michael I.; Sellens, Martin H.; Atienza-Samols, Sui Bi; Pai, Anna C.; Schindler, Joel

doi:10.1007/978-1-4613-3180-3_6

Cited by 6 publications

(2 citation statements)

References 42 publications

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“…The current, popular in vitro attachment assay studies the attachment onto petri dishes coated with various substrates. While this assay has provided a great deal of information about the nature of various matrix proteins that favor attachment, 26,37,38 it has not been instructive about differentiation of the attached trophectoderm. A principal characteristic of attached blastocytes in vivo is their invasiveness that initiates hemochoreal placentation.…”

Section: In Vitro Models: Polarized Epithelial Cellsmentioning

confidence: 99%

Models for the Study of Uterine Receptivity for Blastocyst Implantation

Sharpe-Timms¹,

Glasser²

1999

Semin Reprod Med

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A variety of models have been developed to study endometrial receptivity which involves normal, appropriately timed endometrial development and remodeling for blastocyst attachment and trophoblast invasion during the luteal phase of the menstrual cycle. Due to species differences, the human is by far the best model per se by which to study human endometrial receptivity. Techniques have evolved to obtain in vivo data on endometrial receptivity using hysteroscopy, ultrasonography or magnetic resonance imaging. Despite species differences, comparative studies of mammalian models and tissue- and cell culture models using endometrial tissue or cells harvested at particular phases of the reproductive cycle, or following experimental manipulation, have been used productively to study endometrial function. Differences as well as similarities have proven to be instructive. Such models have been used to study a variety of entities, such as homotypic and heterotypic cell-cell interaction, the role of steroids, cytokines, growth factors, immunomodulatory agents and pharmacological substances. These models have also been used to study cellular, biochemical and molecular mechanisms involved with uterine receptivity. This chapter was designed to provide a critical review of contemporary literature relating to in vivo models and laboratory strategies and paradigms for the study of uterine receptivity for blastocyst implantation.

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Section: In Vitro Models: Polarized Epithelial Cellsmentioning

confidence: 99%

Models for the Study of Uterine Receptivity for Blastocyst Implantation

Sharpe-Timms¹,

Glasser²

1999

Semin Reprod Med

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“…Using this model of trophoblast invasiveness, several investigations have demonstrated that fibronectin, laminin, vitronectin, various collagen forms, thrombospondin and hyaluronic acid are all capable of promoting trophoblast cell adhesion and migration in vitro (Armant et al, 1986a,b;Carson et al, 1987Carson et al, , 1988Sutherland et al, 1988;O'Shea et al, 1990). The adhesive interaction of trophoblast cells with these matrix proteins induces the secretion of specific new proteins by the embryos (Nieder, 1990), as well as a host of other biochemical changes (Sherman et al, 1981). In vitro outgrowth culture of mouse blastocyst-derived trophoblast cells has therefore proven to be an important method for investigating the biochemical basis of primary trophoblast cell differentiation during mouse embryogenesis.…”

mentioning

confidence: 99%

Recombinant entactin promotes mouse primary trophoblast cell adhesion and migration through the Arg-Gly-Asp (RGD) recognition sequence [published erratum appears in J Cell Biol 1993 Jul;122(1):279]

Yelian

Edgeworth

Dong

et al. 1993

The Journal of Cell Biology

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Abstract. In vitro culture of mouse blastocysts during the period coinciding with implantation has revealed that primary trophoblast cells can adhere and migrate in serum-free medium when provided with certain extracellular matrix components, including fibronectin and laminin. Tightly associated with laminin is the glycoprotein, entactin, that may play an important role in basement membrane assembly and cell attachment. Mouse blastocysts were studied using this in vitro model to determine whether entactin was capable of mediating trophoblast invasive activity. Although entactin has never been shown to promote cell migration, we report here that recombinant entactin supported blastocyst outgrowth in a dose-dependent manner, with a maximal effect at 20-50/zg/ml. The ability of trophoblast cells to adhere and migrate on entactin was specifically inhibited by anti-entactin antibody, but not by antibodies raised against laminin. The synthetic peptide, Gly-Arg-Gly-Asp-Ser-Pro, that contains the Arg-Gly-Asp (RGD) integrin recognition site, reversibly inhibited entactin-mediated blastocyst outgrowth in a dose-dependent manner, but had no effect on laminin-mediated outgrowth. The synthetic peptide, Gly-Phe-Arg-Gly-Asp-Gly-Gln, that comprises the actual RGD-containing sequence within entactin, promoted trophoblast outgrowth when immobilized on the substratum. Furthermore, a mutated recombinant entactin, altered to contain a Gin in place of Asp at the RGD site, provided no trophoblast cell adhesive activity. We conclude that entactin promotes trophoblast outgrowth through a mechanism mediated by the RGD recognition site, and that it may play an important role during invasion of the endometrial basement membrane at implantation.

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Protein synthetic requirements for the outgrowth of trophoblast cells from mouse blastocysts

1982

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Mouse blastocysts cultured under optimal conditions attach to the surface of the culture dish and subsequently give rise to outgrowths of trophoblast cells. The migration of trophoblast cells appears to be analogous to their behavior during the invasive phase of implantation in utero. In these studies, we have attempted to determine the time of synthesis and nature of the products required for trophoblast outgrowth. Fourth-day blastocysts were cultured in two different media: cNCTC, a nutrient medium supplemented with fetal calf serum, and PCMF, a simple preimplantation medium lacking amino acids and serum. Trophoblast outgrowth occurs in the former, but not in the latter, medium. Most blastocysts will give rise to outgrowths following as little as 12 hr of exposure to cNCTC at the appropriate time, even if they are subsequently placed in PCMF. Outgrowth fails to occur if blastocysts are treated with cycloheximide during the interval of exposure to cNCTC, whereas treatment with the antimetabolite after the period of culture in cNCTC does not block outgrowth. These observations are consistent with the view that protein(s) essential for trophoblast outgrowth are synthesized many hours prior to the actual event.

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Relationship between the Programs for Implantation and Trophoblast Differentiation

Cited by 6 publications

References 42 publications

Models for the Study of Uterine Receptivity for Blastocyst Implantation

Models for the Study of Uterine Receptivity for Blastocyst Implantation

Recombinant entactin promotes mouse primary trophoblast cell adhesion and migration through the Arg-Gly-Asp (RGD) recognition sequence [published erratum appears in J Cell Biol 1993 Jul;122(1):279]

Protein synthetic requirements for the outgrowth of trophoblast cells from mouse blastocysts

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