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PubMed1993

Increased depth of trophoblast invasion after chronic constriction of the lower aorta in rhesus monkeys.

OBJECTIVE: Our purpose was to investigate whether a reduction in uteroplacental perfusion pressure would produce changes in trophoblast-uterine interactions at the cellular level. STUDY DESIGN: Strictures were placed around the abdominal aortas of rhesus monkeys at 116 +/- 7 days of pregnancy to reduce uteroplacental perfusion pressure. Placental bed biopsy specimens were obtained at cesarean section, and cytotrophoblasts were identified by means of an anticytokeratin antibody. RESULTS: In monkeys without aortic strictures, interstitial trophoblast invasion was restricted to the outer half of the endometrium. Endovascular trophoblast invasion involved the entire endometrial portion of uterine vessels and extended through the subjacent half of their myometrial segments. In seven of nine monkeys with aortic strictures the depth of interstitial trophoblast invasion was substantially increased and extended throughout the entire decidua and at least a portion of the myometrium. In contrast, the pattern of endovascular trophoblast invasion was identical to that observed in the placental beds of control animals. CONCLUSION: These results suggest that uteroplacental perfusion pressure or oxygen content may be important physiologic factors controlling the depth of interstitial cytotrophoblast invasion.

Animals↗
PubMed1994

Ethanol enhancement of ligand-stimulated cAMP production by cultured human placental trophoblasts.

Chronic ethanol (EtOH) use during pregnancy can be associated with fetal injury including the fetal alcohol syndrome (FAS). A contributing factor in this fetal injury may be the effect of EtOH on the placenta. In this study, we have examined the effect of in vitro EtOH treatment on adenosine 3':5'-cyclic monophosphate (cAMP) production by cultured trophoblasts, in response to various ligands. Epinephrine (10(-6) M) rapidly stimulated cAMP with a peak between 2.5 and 5 min, which gradually returned to basal levels over 3-4 hr. EtOH treatment for > 16 hr resulted in an up-regulation of epinephrine-stimulated cAMP production. Inhibition of phosphodiesterase with Rolipram enhanced the effect of EtOH on cAMP production, suggesting that the effect of EtOH treatment was not due to phosphodiesterase inhibition. In cultured trophoblasts, EtOH treatment increased both epinephrine and 16,16'-dimethylprostaglandin E2 (dm-PGE2)-dependent cAMP production at varying ligand concentrations, suggesting an increased capacity to respond. When trophoblasts were treated with forskolin, a stimulator of adenylyl cyclase, cAMP production was enhanced in EtOH-treated cells. This suggests that EtOH treatment enhances adenylyl cyclase activity in these intact, cultured cells. Unlike trophoblasts from term human placenta, JAR choriocarcinoma cells did not respond to epinephrine, adenosine, or dm-PGE2. The choriocarcinoma cells appeared to have lost the ability to respond to these ligands. Although the JAR cell adenylyl cyclase was stimulated by forskolin, EtOH treatment did not alter forskolin-stimulated cAMP production. In summary, EtOH-induced up-regulation of cAMP production appears to be cell specific, being present in normal human trophoblasts but not in undifferentiated choriocarcinoma cells.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Altered trophoblast functions in implantation-defective mouse embryos.

Extracellular proteases, such as plasminogen activator (PA), may play a role in the invasive action of trophoblasts during blastocyst implantation in mice. Detailed analysis of proteases released by trophoblasts must be carried out in culture for practical reasons, but the in vitro results should ideally be related to implantation in utero to test the validity of the conclusions in the model system. The implantation-defective mutant (tw73) allows us to investigate alterations of trophoblasts in culture which will reflect their altered functions in utero. The trophoblasts of mutant embryos attached and proliferated in culture to the same extent as control embryos. Therefore, the mutant effect is not to kill or stop the division of these cells. However, trophoblasts of tw73 homozygotes showed decreased invasive ability when transplanted into testes. To examine the biochemical basis of altered invasive behavior in mutants, PA activity released by blastocysts in culture was measured. Medium conditioned by tw73 homozygotes contained less PA fibrinolytic activity than culture medium of control embryos. The correlation between decreased in vitro PA activity and the invasive defects seen in utero and ectopically, supports the involvement of PA in the invasive phase of the implantation process.

Animals↗
PubMed1990

Hydatidiform mole: clinicopathologic associations with the development of postevacuation trophoblastic disease.

Clinical information and histopathologic material for 165 patients with hydatidiform mole referred to the John I. Brewer Trophoblastic Disease Center of Northwestern University Medical School during one year were reviewed in order to identify characteristics more likely to be associated with the development of gestational trophoblastic tumors. Twenty-nine patients (18%) required chemotherapy for invasive mole or choriocarcinoma. Patients with uterine enlargement beyond that expected for dates and patients with ovarian theca-lutein cysts were much more likely to require treatment after molar evacuation (47% vs. 18% and 40% vs. 16%, respectively). There was no correlation between the initial human chorionic gonadotropin level, gestational age, uterine size per se, maternal age or gravidity and the subsequent clinical course. Histologically, the following factors were associated with an increased incidence of postmolar gestational trophoblastic tumor: (1) progressive nuclear atypia (26.7% if atypia present vs. 40% if absent); (2) necrosis and hemorrhage (39.1% if extensive vs. 12.8% if limited); (3) decreased trophoblast maturation (48% if less than 20% mature vs. 8.7% if greater than or equal to 20% mature); (4) trophoblast proliferation (50% if marked vs. 13.9% if limited); (5) increased ratio of cytotrophoblast to syncytium (33.3% if greater than 1 vs. 6.4% if less than 1); and (6) absence of Nitabuch's layer (21.4% if absent vs. 11.6% if present). Hydatidiform moles which demonstrate clinical or histopathologic evidence of excessively abnormal proliferative activity, as indicated by these features, are more likely to develop invasive mole or choriocarcinoma and should be considered for prophylactic chemotherapy.

Adolescent↗
PubMed1988

Developmental regulation of the monoclonally defined IIC3 antigen during primary and secondary trophoblast differentiation in vitro.

The monoclonally defined IIC3 antigen has been found to be developmentally regulated during primary and secondary trophoblast differentiation in the mouse. Cell surface expression of the antigen was associated only with diploid and tetraploid trophoblast cell types. Endoreduplication to 8C DNA in differentiating trophoblast giant cells was associated with a loss of IIC3 cell surface expression and appearance of cytoplasmic expression. This developmental change was not temporally regulated, but dependent on the attachment and outgrowth of the trophoblast in vitro. The surface antigen was neither shed into the media nor masked by glycosylation, but was apparently internalized by the trophoblast giant cells.

Animals↗
PubMed1986

Indomethacin inhibits the uptake of 22sodium by ovine trophoblastic tissue in vitro.

Blastocysts from several species synthesize prostaglandins in vitro, but the exact functions of the prostaglandins are unknown. The purpose of this study was to determine if indomethacin, an inhibitor of prostaglandin synthesis, would inhibit the uptake of 22sodium ([22Na]) by ovine trophoblastic tissue. To determine the concentration of indomethacin that would inhibit the synthesis of PGF2 alpha and 13,14-dihydro-15-keto-PGF2 alpha (PGFM) by blastocysts, blastocysts were collected from ewes 16 days after mating, sliced into pieces approximately 2 mm in length and incubated for 48 h at 37 degrees C in 2 ml of medium containing either 0, 0.2, 0.4, 0.8 or 1.6 mM of indomethacin. Concentrations of indomethacin greater than or equal to 0.2 mM reduced (P less than .01) trophoblastic release (ng/micrograms DNA) of PGF2 alpha from 205 +/- 71.2 to less than or equal to 3.3 +/- 0.2, reduced PGFM from 0.7 +/- 0.1 to less than or equal to 0.17 +/- 0.01, and inhibited formation of trophoblastic vesicles. In a second experiment, blastocysts were recovered from ewes 16 days after mating and pieces of trophoblast were incubated with [22Na] and either 0 or 0.4 mM of indomethacin. Indomethacin reduced the uptake of [22Na], which is an indirect measure of the transport of water across epithelia, from 3680 +/- 1118 to 934 +/- 248 cpm/micrograms DNA (P less than .03) and prevented formation of trophoblastic vesicles. Prostaglandins produced by ovine blastocysts might be involved in controlling uptake of water, which is essential for expansion of blastocysts.

Animals↗
PubMedDate not supplied

Characteristics of trophoblastic tissue derived from in vitro culture of preimplantation embryos of the common marmoset monkey.

The features of trophoblastic tissue derived from the in vitro culture of marmoset monkey embryos have been described. Long-term trophoblast cultures (in excess of three years in one case) were established from the primary trophoblast monolayer of four of 38 embryos; division of one of these embryos produced two long-term cultures. The trophoblast cells retained their ability to synthesize and secrete chorionic gonadotrophin (CG) during maintenance in vitro and were capable of prolonging the luteal phase when transferred to the uterus of marmosets. A characteristic feature of the cultures was the formation of multiple fluid-filled vesicles enclosed by a single layer of cytotrophoblast cells and attached to the culture dish by a small monolayer of syncytiotrophoblast cells. The tissue was propagated by cutting vesicles into small pieces and placing into a fresh culture dish; attempts to subculture using single-cell suspensions were unsuccessful. These cultures provide a convenient source of marmoset CG for purification as well as an in vitro system for studying other secretory products of primate trophoblast.

Animals↗
PubMedDate not supplied

Coincubation--an experimental approach to the study of decidual-trophoblast interaction.

Coincubation of trophoblast and decidual tissue explants was used for the study of placental-endometrial interaction in early pregnancy. To this end two types of experiments were performed: coincubation with (type A) and without (type B) direct tissue contact. The rate of incorporation of [14C]leucine into cytosol proteins in both tissues was employed for the estimation of total protein synthesis. Prolactin production in vitro was used as a specific marker of the decidual and hCG of the trophoblast cell function. The results show that the type A coincubation experiments produced a strong inhibition of cytosol protein synthesis in both tissues. PRL production by the decidual tissue and hCG production by the trophoblast tissue was reduced. In the type B coincubation experiments protein synthesis and prolactin production by the decidual tissue remained within the control range. In the trophoblast tissue explants protein synthesis and hCG production were depressed. The degree of inhibition was, however, lower than that in type-A experiments. Based on these results it was concluded that the in vitro model of coincubation of trophoblast and decidual tissue explants is suitable for the study of the role of tissue interactions in vitro.

Chorionic Gonadotropin↗
PubMedDate not supplied

Immunohistochemical studies of fetal trophoblast and maternal decidua in hydatidiform mole and choriocarcinoma.

Immunohistochemical techniques have been used to investigate the expression of fetal trophoblast antigens and the maternal leucocytic response in molar pregnancy and choriocarcinoma. The antigenic phenotype of morphologically defined trophoblast populations in complete, partial and invasive moles was analogous to that in normal pregnancy. All trophoblast phenotypes described in normal pregnancy were also identified in choriocarcinoma, suggesting that extensive differentiation into heterogeneous subgroups occurs in malignant trophoblast. The maternal leucocytic infiltrate in molar pregnancy consisted of T lymphocytes and class II MHC-positive macrophages. CD2-positive, CD3-negative lymphocytes were identified in molar decidua but not in uterine tissue in choriocarcinoma. Similarly, endometrial granulocytes were present in molar decidua but not in choriocarcinoma; these cells were associated with decidualization rather than with fetal trophoblast.

Choriocarcinoma↗
PubMed1994

C-myc and tumour suppressor gene product expression in developing and term human trophoblast.

Proliferation and differentiation of villous trophoblast during placental development, from an early stage to full-term, were investigated in routinely fixed and processed tissues, by means of the immunocytochemical localization of the cell cycle-related proto-oncogene c-myc and the p53 and retinoblastoma susceptibility (Rb) tumour-suppressor gene products. The proliferative activity of the trophoblast was determined using an antibody against proliferating cell nuclear antigen (PCNA) which stains all proliferating cells in paraffin-embedded tissues. Diffuse nuclear immunoreactivity for PCNA, c-myc and Rb gene products was a consistent finding in early cytotrophoblast; c-myc product expression was also detectable in both layers of mid-gestation trophoblast. Only scattered cytotrophoblastic nuclei of early gestational placenta displayed immunostaining for p53 gene product. In full-term placenta c-myc expression was undetectable while Rb gene product and PCNA immunoreactivity declined markedly. These results indicate that the expression of the above genes is spatio-temporally regulated during placental development. A potential involvement of the oncosuppressor gene products p53 and Rb in the control of trophoblastic proliferation and of c-myc in the control of both the proliferative and differentiation pathways of trophoblastic cells is suggested.

Cell Division↗
PubMed1991

Unique features of the trophoblast interferons.

The trophoblast interferons (IFN) are Type I IFN with about 50% amino acid sequence identity to the leukocyte IFN (IFN-alpha). They are the major secretory products of the trophoblast of ruminant ungulate species during pregnancy in the period immediately preceding attachment and implantation when they have been implicated in the phenomenon known as maternal recognition of pregnancy. The trophoblast IFN have antiviral and antiproliferative activities typical of other Type I IFN, but unlike IFN-alpha, -beta and -omega are poorly responsive to viral induction and have a highly restricted pattern of expression. Nevertheless, a recombinant bovine IFN-alpha can mimic many of the properties of the trophoblast IFN and has been used pharmacologically to improve pregnancy success in sheep. It still remains unclear, however, whether the trophoblast IFN have unique biological properties or whether they are unusual merely by virtue of the location, magnitude and temporal nature of their expression at a critical time during pregnancy.

Animals↗
PubMed1987

Class I major histocompatibility complex antigen expression on early murine trophoblast and its induction by lymphokines in vitro.

The expression of paternal class I and class II major histocompatibility complex (MHC) antigens in cultures of murine ectoplacental cone trophoblast was examined using immunogold labelled antibodies and electron microscopy. Class I MHC antigens could be induced on ectoplacental cone derived trophoblast following exposure to concanavalin A stimulated T cell supernatants. Class I MHC antigens were not detected in untreated trophoblast cultures. Class II MHC antigens were never detected on trophoblast whether treated or untreated. This is the first report of the experimental induction of Class I MHC antigens on a population of normally MHC-negative trophoblast cells.

Animals↗
PubMed1991

Differential expression of complement regulatory proteins on subpopulations of human trophoblast cells.

Trophoblast cells forming the reactive interface between the mother and her semiallogeneic fetus risk attack by cellular and humoral elements of the maternal immune system. Biochemical, molecular, and immunohistologic studies have identified membrane cofactor protein (MCP) and decay accelerating factor (DAF) on trophoblast cells, which could assist in preventing lysis of the cells by complement-activating maternal antibodies. In this immunocytochemical study, differential expression of these two members of the family of complement regulatory proteins on subpopulations of human trophoblast cells and other types of cells in first and third trimester placentas was demonstrated. Staining with anti-MCP was particularly strong on villous cytotrophoblast cells and giant cells in first trimester tissues in comparison with other types of cells. In contrast, staining with anti-DAF was strong on proliferating cytotrophoblast in first trimester tissues, and on basal plate cytotrophoblast and decidual cells in term tissues. Placental villous mesenchymal cells but not trophoblast cells expressed a third regulatory protein, complement receptor 1. These observations support the postulate that complement regulatory proteins are critical to protection of the fetal allograft, and suggest specific requirements for trophoblast cells according to stage of differentiation and anatomic location.

Antigens, CD↗
PubMed1992

Evidence for the expression of granulocyte-macrophage colony-stimulating factor receptors by human first trimester extravillous trophoblast and its response to this cytokine.

The present study has demonstrated that human extravillous trophoblast cells isolated from first trimester placentae can bind granulocyte-macrophage colony-stimulating factor (GM-CSF). We have used a technique which incorporates a phycoerythrin (PE)-conjugated GM-CSF in association with a monoclonal antibody against trophoblast (BC-1) in single and double flow cytometric analysis. Trophoblast cells are also observed to show increased DNA synthesis in response to GM-CSF as assayed by [3H]thymidine incorporation and proliferative activity as demonstrated by double immunocytochemical staining of cells with a trophoblast cytokeratin marker (PKK1) and for the nuclear proliferation antigen (Ki-67). These findings provide evidence that human extravillous trophoblast expresses receptors for GM-CSF and responds to this cytokine.

Antibodies, Monoclonal↗
PubMed1992

PGE2-independent immunosuppressive activity of horse trophoblast tissue.

It has been proposed that PGE2 is an important immunosuppressant acting at the fetal-maternal interface during pregnancy. We have previously shown that horse conceptus-conditioned medium suppresses lymphocyte proliferation. This experiment was designed to determine if horse conceptus-derived immunosuppressive activity could be attributed to PGE2 production by the trophoblast tissue. Trophoblast tissue from 21-day-old conceptuses was cut into equal sections and cultured in the presence or absence of the prostaglandin inhibitor, indomethacin. Following culture, immunosuppressive activity and the concentration of PGE2 were determined for each sample of both horse-trophoblast conditioned medium (HTCM) and indomethacin-treated HTCM (I-HTCM). Suppressive activity was identified in lymphocyte proliferation assays via reduced [3H]thymidine uptake by pokeweed mitogen stimulated horse lymphocytes. A radioimmunoassay was used to quantify PGE2. While PGE2 production was greatly reduced in cultures containing indomethacin, trophoblast-derived immunosuppressive activity was not affected. These data indicate that PGE2 is not the primary immunosuppressant produced by horse trophoblast tissue.

Animals↗
PubMed1993

Inhibitory effect of choriocarcinoma-derived high molecular weight factor (HMWF) on lymphocyte proliferation and adhesion to trophoblasts.

Trophoblast-secreted soluble factors may deter the immune rejection of the fetus which can occur from interaction between maternal lymphocytes and fetal trophoblasts in decidua. The effect of size-fractionated culture fluid of choriocarcinoma cells on the function of lymphocytic cells was studied. The results show that dialyzed soluble factor (HMWF) of molecular weight > 100 kDa was inhibitory to lymphocyte proliferation in a dose-dependent manner and prevented lymphocyte-to-trophoblast adhesion in a similar fashion. The effect was abrogated by a freezing-thawing process and heat treatment. Similarly, the fractions below 100 kDa size had no effect on lymphocyte functions. Although the nature of HMWF is not yet known, it appears that this factor differs from most of the well-characterized pregnancy factors but is similar to the recently described high molecular weight factor found in primary cultures of trophoblasts and choriocarcinoma lines. The inhibitory effect of trophoblast-derived HMWF on cell-contact-based immune recognition may contribute to maternal tolerance.

Analysis of Variance↗
PubMed1994

Demonstration of the low affinity alpha subunit of the granulocyte-macrophage colony-stimulating factor receptor (GM-CSF-R alpha) on human trophoblast and uterine cells.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a classical haematopoietic cytokine which has also been implicated in placental growth and development. In this study we have performed a detailed immunohistological localization of the low affinity GM-CSF receptor (GM-CSF-R alpha) in human first trimester implantation site and non-pregnant endometrium. We have also investigated receptor expression and GM-CSF binding in vitro by normal first trimester trophoblast using flow cytometric analysis and compared this with JEG-3 and JAR choriocarcinoma cells. In the first trimester, the GM-CSF-R was found to be present on villous cytotrophoblast and all populations of extravillous trophoblast. Expression by villous syncytiotrophoblast was weak or absent, but this increased markedly by term. GM-CSF-R were also expressed by fetal Hofbauer cells within the mesenchyme of the chorionic villi and by uterine glandular epithelium and decidual macrophages within maternal decidua. GM-CSF-R was not expressed by glands in proliferative phase endometrium but began to appear during the secretory phase, suggesting hormonal regulation of the receptor on uterine glandular epithelium. Flow cytometric comparison of normal isolated first trimester trophoblast and JEG-3 and JAR choriocarcinoma cells revealed two- to threefold higher surface expression of GM-CSF-R by choriocarcinoma cells and higher binding capacity for rhGM-CSF than normal trophoblast. These results suggest that GM-CSF may regulate growth and development of human trophoblast. GM-CSF may also influence placental development and function by acting via decidual and fetal macrophages, and uterine glandular epithelium, which are the other cell populations to express the receptor.

Choriocarcinoma↗
PubMed2005

Neospora caninum: antibodies directed against tachyzoite surface protein NcSRS2 inhibit parasite attachment and invasion of placental trophoblasts in vitro.

Polyclonal and monoclonal antibodies to native Neospora caninum tachyzoite surface protein NcSRS2 were generated and tested in vitro for their ability to neutralize tachyzoite attachment to and invasion of host cells. Host cells included Vero cells and a newly cloned, immortalized ovine trophoblast cell line obtained from primary cultures of ovine placenta. The ovine trophoblasts had morphology consistent with fetal trophoblasts and expressed mRNA for interferon-tau, a marker for trophoblasts. Native NcSRS2 was used to immunize mice to obtain monospecific anti-NcSRS2 polyclonal serum and anti-NcSRS2 monoclonal antibodies. Compared to irrelevant antibodies, monospecific anti-NcSRS2 serum and two anti-NcSRS2 monoclonal antibodies, 100.2.4.4 and 119.4.9.10, significantly blocked invasion of tachyzoites into both trophoblasts and Vero cells. Parasite attachment, assessed by IFA, was significantly reduced by anti-NcSRS2 mAb 100.2.4.4 and monospecific serum. The findings provide rationale to investigate a role for antibodies to NcSRS2 in prevention of N. caninum transplacental transmission in vivo.

Animals↗