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PubMed1993

Cell proliferative activity and mutation of P53 suppressor gene in human gestational trophoblastic disease.

Cell proliferative activity and the overaccumulation of P53 suppressor gene were evaluated in 26 cases of gestational trophoblastic disease and five cases with normal placentae. Formalin-fixed, paraffin-embedded histological sections were used for immunohistochemistry, utilizing the avidin-biotin-peroxidase technique and antibodies to PCNA (proliferative cell nuclear antigen) and to P53 (product of suppressor gene). Positive reactions for PCNA were graded from 1+ to 3+ (1(+)-less than 10% of cells; 2(+)-10-50%; 3(+)-more than 50%). Eight of 10 cases of choriocarcinoma (80%) showed moderate to strong reactivity for PCNA (2+ and 3+). All 9 cases with hydatidiform mole and 6 of 7 cases with partial mole also demonstrated 2+ and 3+ reactions for PCNA. There was minimal or no PCNA staining in the trophoblastic cells of normal placentae. Five of 10 cases with choriocarcinoma (50%) exhibited P53 overaccumulation as did 7 of 9 cases with hydatidiform mole (78%). In hydatidiform moles, P53 staining was limited to the areas of trophoblastic proliferation separate from chorionic villi. None of the partial moles or normal placentae showed P53 overaccumulation. It is concluded that the cell proliferative activity of choriocarcinomas as well as complete and partial hydatidiform moles are comparable. On the other hand, the mutation of P53 suppressor gene, as demonstrated by the overaccumulation of P53 protein, is seen only in true trophoblastic neoplasms, namely, choriocarcinomas and hydatidiform moles.

Antigens, Neoplasm↗
PubMed1997

Expression of c-fos and jun protooncogenes in ovine trophoblasts in relation to interferon-tau expression and early implantation process.

Expression of c-fos and jun protooncogenes was analyzed in the ovine extraembryonic trophoblast from days 14-18 of gestation, using Northern and Western blotting and immunohistochemistry. This study was carried out in relation to the early implantation process and the expression of interferon-tau, which is secreted in large amounts for a few days before implantation. Our results demonstrated that c-fos, c-jun, and junB were differently expressed in the ovine trophoblast around the time of implantation. The c-fos mRNA and protein were detected at high levels prior to attachment and decreased thereafter, following the pattern of expression of interferon-tau, whereas c-jun expression was maintained at relatively high levels during the implantation process. By contrast, the levels of junB mRNA and protein decreased prior to attachment. Immunohistochemical studies indicated that JunB, like C-Fos and interferon-tau, was no longer expressed in the trophoblastic cells which had established cellular contacts with the uterine epithelium. A striking finding in this study is the temporal correlation between the accumulation of c-Fos and c-Jun proteins and the expression of the interferon-tau (days 14 and 15 of gestation). We also showed by gel-retardation assays that an AP-1-like site present in the promoter of one interferon-tau gene was functional in vitro, as judged by its ability to bind day-15 trophoblast nuclear protein extracts. Nuclear proteins binding to this site had the characteristics of AP-1, as judged by the ability to be competed efficiently by a consensus TRE (12.0-tetradecanoyl phorbol 13-acetate-responsive element)-site oligonucleotide and by antibodies to c-Fos and Jun proteins. These results suggest that Fos and Jun could form regulatory complexes of interferon-tau expression and/or are regulated by common mechanisms which are still unknown.

Animals↗
PubMed1999

Trophoblast giant cells express NF-kappa B2 during early mouse development.

To investigate whether transcription factors of the NF-kappa B family could play a role in early mammalian development, we have analyzed the expression of nfkb1, nfkb2, c-Rel, RelA, RelB, and bcl-3 from 6.5- to 10.5-day mouse embryo implantation sites. Our study shows that nfkb2 mRNA and protein are specifically localized in trophoblast giant cells throughout the stages analyzed. Trophoblast giant cells obtained upon in vitro cultures of 7.5-day ectoplacental cones display NF-kappa B DNA-binding activity that is supershifted by the anti-NF-kappa B2 antibody. Trophoblast giant cells are embryo-derived cells that form an interface between embryonic and maternal tissues during early mouse development; they are involved in decidual remodeling and expansion of the embryonic cavity, placenta formation, and possibly avoidance of maternal immune response to the embryo. Our study suggests that NF-kappa B2 could play a role in the modulation of genes expressed in trophoblast giant cells during the course of early embryogenesis, and therefore be relevant for tissue remodeling and morphogenesis of placenta.

Animals↗
PubMed1977

Criteria of complete remission from trophoblastic neoplasia with the use of human chorionic gonadotropin (HCG) excretion pattern as a parameter.

The excretion pattern of human chorionic gonadotropin (hCG) or luteinizing hormone (LH) was observed in the urine of 77 patients with trophoblastic neoplasia, 109 with complete remission from trophoblastic neoplasia, and 94 with no trophoblastic neoplasia, when the anti-beta-subunit hCG system radioimmunoassay (anti-beta-subunit RIA), which specifically measured hCG was used. The sensitivity of anti-beta-subunit RIA was limited to urinary hCG 16 mIL/ml from the specificity of the anti-beta-subunit serum. Luteinizing hormone in the urine of patients with complete remission and in normal menstrual, postmenopausal, and castrated women was less than 16 mIU/ml in most cases. The excretion pattern of urinary hCG in the patients undergoing treatment for trophoblastic neoplasia was more clearly comprehended with the anti-beta-subunit RIA as compared with the anti-hCH RIA. The criteria for judgment of complete remission were that the hCG value dropped to less than 16 mIU/ml and that cellular response was not observed at least in the last two courses.

Adult↗
PubMed1994

Vascular patterns of gestational trophoblastic tumors by color Doppler ultrasound.

BACKGROUND: Destruction of uterine vasculature is a common phenomenon in gestational trophoblastic tumors. The authors categorized such uterine vasculature by color Doppler ultrasound and studied its clinical significance. METHODS: Color Doppler ultrasound was performed in 28 patients with gestational trophoblastic tumors. The vascular morphologic manifestations were recorded, and the peak systolic velocity and resistance index of uterine artery were calculated. Serum beta-human chorionic gonadotropin (hCG) levels were measured periodically to monitor chemotherapy response. Seventeen uneventful postmole uteri were used as controls. Two-tailed Student's t-test and Fisher's exact test were used for statistical analysis. RESULTS: The gestational trophoblastic tumors were categorized as diffuse type (N = 7), lacunar type (N = 16), and compact type (n = 5) according to their vascular patterns. The mean serum beta-hCG level at diagnosis in diffuse type lesions (6608 +/- 6320 mIU/mL) was significantly lower than in the lacunar type (40462 +/- 39735 mIU/mL; P = 0.04) and compact type (212114 +/- 205126 mIU/mL; P = 0.02), whereas the level in compact type lesions was significantly higher than in the lacunar type (P = 0.003). Lacunar type lesions exhibited a significantly lower uterine artery resistance index (0.51 +/- 0.13) than diffuse type (0.66 +/- 0.10; P = 0.03) or compact type lesions (0.70 +/- 0.06; P = 0.02). All lesions exhibited significantly higher peak systolic velocity than control subjects (P < 0.001); however, no significant difference was observed among them. Brief courses (< 5 cycles) of chemotherapy cured more diffuse type (6 of 7) than lacunar type (3 of 15, P = 0.006) or compact type lesions (0 of 5, P = 0.008). Histopathologic diagnosis was available for 11 lesions. They were invasive mole in seven lacunar type lesions and choriocarcinoma in four compact type lesions. CONCLUSION: Vascular morphologic patterns of gestational trophoblastic tumors by color Doppler ultrasound correlated well with beta-hCG levels, uterine hemodynamics, chemotherapy response, and possibly the histopathologic diagnosis.

Arteries↗
PubMed2000

Antiphospholipid antibodies affect trophoblast gonadotropin secretion and invasiveness by binding directly and through adhered beta2-glycoprotein I.

OBJECTIVE: To investigate the in vitro ability of antiphospholipid antibodies (aPL) to bind human trophoblast cells and to affect gonadotropin secretion and invasiveness. METHODS: Antiphospholipid antibody IgG from women with recurrent miscarriages, beta2-glycoprotein I (beta2GPI)-independent IgG aPL human monoclonal antibody (mAb) (519), and IgM anti-beta2GPI human mAb (TMIG2) were investigated for their binding to trophoblasts cultured for various amounts of time, their ability to affect invasiveness of Matrigel-coated filters, and their release of human chorionic gonadotropin (hCG). RESULTS: Polyclonal IgG aPL, as well as mAb 519 and TMIG2, bound to trophoblasts, the highest binding being found when cells displayed the greatest amount of syncytium formation. TM1G2 binding was found to be betaGPI dependent. Both polyclonal and monoclonal aPL, but not the controls, significantly reduced hCG release and Matrigel invasiveness. CONCLUSION: These findings suggest that aPL recognition of both anionic PL and adhered beta2GPI on trophoblast cell structures might represent a potential pathogenetic mechanism for defective placentation in women with the antiphospholipid syndrome.

Anions↗
PubMed1981

Morphodynamics of outgrowths of mouse trophoblast in the presence and absence of a monolayer of uterine epithelium.

Mouse blastocysts were cultured in the presence and absence of a confluent uterine, luminal, epithelial monolayer in order to assess (10 comparative developmental abilities and (2) the existence and nature of embryo-uterine intercellular contacts. Embryonic development and mural trophoblast outgrowth were examined by light, transmission and scanning electron microscopy, and by time-lapse cinematography. The results demonstrate that cultured mouse blastocysts are capable of development that is essentially equivalent to the early egg cylinder stage in the presence and absence of a uterine epithelial substratum. Penetration of the endometrium and displacement of uterine luminal epithelial cell in vivo is paralleled in vitro by the displacement of uterine cells from the advancing edge of outgrowing mural trophoblast. The ability of mural trophoblast to continue to outgrow and displace uterine cells persists for a finite period of time. The findings are discussed with respect ot (1) the nature of embryo-uterine contact in vivo and (2) mechanisms proposed to explain trophoblastic displacement of uterine luminal epithelial cells during normal implantation.

Animals↗
PubMed1991

Trophoblast-uterine interactions during equine chorionic girdle cell maturation, migration, and transformation.

The structure of the equine chorionic girdle between days 28 and 42 of gestation was examined. Of particular interest were differentiation of trophoblastic cells within the girdle, adhesion between girdle and endometrium, invasion and displacement of the uterine epithelium, and the nature of the endometrium when girdle cells migrate into it to form endometrial cup cells. The chorionic girdle, identified initially as a band of tall columnar cells, becomes a stratified columnar epithelium indented by clefts and pits. Adhesion to and penetration through the endometrial luminal epithelium are rapid and occur initially in very limited areas. Stromal invasion occurs as strands of contiguous trophoblast cells invade through the basal lamina. Only girdle cells that are adjacent to the basal lamina or have entered the endometrial stroma undergo hypertrophy and differentiate into cup cells. At the initiation of trophoblastic invasion, the luminal epithelium contains numerous, large, intraepithelial, granular lymphocytes; small lymphocytes then accumulate in the stroma, but by day 42 lymphocytes are largely confined to the periphery of the cup. Although adhesion of trophoblast to the endometrial surface is initiated by small groups of girdle cells on restricted areas of the endometrial folds, the area is then increased by new areas of adhesion and by expansion of the initial invasion. Areas of girdle cells that do not attach undergo necrosis, as do superficial portions of areas of invasion. Consequently the girdle cells that form cups may be a minority of the original population. It is suggested that the differentiation of girdle cells is closely programmed and that cells that do not reach the stroma become necrotic at the same time that endometrial cup cells are differentiating.

Animals↗
PubMed1985

Distribution and characterization of anionic sites in trophoblast and capillary basal laminas of human placental villi.

The distribution of anionic sites was studied in the trophoblastic and fetal capillary basal laminas of developing human placental villi with the cationic stain ruthenium red. At 7-12 weeks of gestation the trophoblastic basal lamina (TBL) contained ruthenium red-positive granules in a quasi-regular array throughout the lamina densa or sometimes concentrated at the interstitial surface of the lamina densa. The capillary basal lamina (CBL) (and anionic sites) were not present at this age. Anionic sites were also associated with collagen or reticular fibrils. At term, the TBL was largely devoid of anionic sites except for some distributed along its interstitial surface. The CBL was present in later gestation and sometimes had arrays of anionic sites. In order to characterize the anionic sites, minced pieces of villi were incubated in the presence or absence of either chondroitinase ABC, heparitinase, neuraminidase, or Streptomyces hyaluronidase in appropriate buffer systems. Incubation of early villi with heparitinase resulted in the disappearance of the TBL-associated sites. Chondroitinase ABC appeared to reduce staining of collagen-associated sites. In term villi, heparitinase removed those few sites still associated with the TBL but did not affect sites associated with the CBL or collagen. Chondroitinase ABC resulted in the disappearance of all anionic sites. In later gestation, a number of developmentally important macromolecules are transported across the trophoblast and enter the fetal capillaries. We conclude that the absence of an array of polyanionic sites from the term placenta TBL and the reduction in the amount of extracellular matrix intervening between the trophoblast and capillaries are adaptations to enhance the exchange of macromolecules across the placenta.

Anions↗
PubMed1982

Isolation and characterization of polyoma virus mutants which grow in murine embryonal carcinoma and trophoblast cells.

Mouse trophoblast cell lines established from cultured midterm placenta and a cell line obtained from cultured blastocyst resemble trophectoderm cells. These cells are resistant to infection by wild-type polyoma virus. We have isolated six polyoma virus mutants capable of growing in trophoblast cell lines. Restriction enzyme analyses and marker rescue experiments revealed that the genetic changes necessary for the growth of these mutants ( PyTr mutants) in trophoblast cells were located in a regulatory region of the genome between the origin of viral DNA replication and the region encoding the viral structural proteins. PyTr mutants are, therefore, similar to PyEC mutants, described by others, which are able to grow in embryonal carcinoma cell lines such as F9 or PCC4. The nucleotide sequence of two independently obtained PyTr mutants has an identical 26-bp deletion from nucleotide 5131 to 5156. This deleted region is replaced by either the sequence GGGA or by viral DNA sequences that flank this deletion. PyECF9 mutants grow well in trophoblast and trophectoderm cells, but PyTr mutants do not grow in F9 or PCC4 cells.

Animals↗
PubMed2002

Color Doppler imaging in the sonohysterographic diagnosis of residual trophoblastic tissue.

PURPOSE: The purpose of this study was to evaluate the role of color Doppler imaging during sonohysterography in the diagnosis of residual trophoblastic tissue. METHODS: This prospective cohort study involved 25 consecutive women with clinical and sonographic signs of an echogenic intrauterine mass who were referred to the sonography unit of our institution for evaluation. All women underwent saline infusion sonohysterography with color Doppler sonographic evaluation. An operative hysteroscopy with histologic examination was performed in 17 cases. RESULTS: Thirteen women (group A) had sonohysterographic features suggestive of residual trophoblastic tissue (ie, an echogenic intrauterine lesion not detached from the uterine wall after introduction of saline). The initial diagnosis was confirmed by histologic analysis in all cases. Blood flow was detected within the intrauterine mass in 6 (46%) of these 13 women; the resistance indices were low in all 6 cases (mean +/- standard error, 0.38 +/- 0.01). Twelve women (group B) had sonohysterographic findings negative for retained tissue, and no blood flow was detected within any of the intrauterine masses in this group (p < 0.05). CONCLUSIONS: Our results confirm the potential role of color Doppler sonography in the initial diagnosis of residual trophoblastic tissue. The detection of color Doppler signals, especially with low-resistance flow, within an intrauterine lesion should increase the confidence of the sonologist in the diagnosis of residual trophoblastic tissue.

Adult↗
PubMed2003

Development of the utero-placental circulation: the role of carbon monoxide and nitric oxide in trophoblast invasion and spiral artery transformation.

It is now well known that in order to establish human hemochorial placentation and to provide a progressive increase in blood supply to the growing fetus, the uterine spiral arteries must undergo considerable alterations. This physiological modification is thought to be brought about by the interaction of invasive cytotrophoblast with the spiral artery vessel wall. Despite intensive research our understanding of the mechanisms that control human trophoblast invasion in normal, let alone abnormal pregnancy, are sill poorly understood. This is partly due to difficulties in obtaining "true" placental bed biopsies and most investigators have relied on in vitro models of trophoblast invasion. This article describes the morphological changes that occur within the placental bed throughout human pregnancy along with a review of the various studies which have attempted to sample the placental bed. Thereafter, follows a review of the evidence that invasive trophoblast can release the vasoactive agents nitric oxide and/or carbon monoxide which, in turn, could contribute to early physiological changes in spiral arteries prior to destruction of the smooth muscle within the vessel wall. Current evidence supports the idea that trophoblast-derived carbon monoxide may contribute to spiral artery modification. In contrast there is no evidence for a similar role by nitric oxide.

Arteries↗
PubMed1993

Structural interactions of trophoblast and uterus during hemochorial placenta formation.

It is argued that the successful placental arrangements are those that decrease the exposure of the trophoblast to the efferent side of the cellular immune response. Examples are taken from three different groups with hemochorial placentation, to show that their placental morphology places most of the trophoblast in contact with maternal blood, not maternal connective tissue. In addition, maternal cells of the junctional area are modified either before contact with trophoblast (rat) or just after trophoblast invasion (primate), or the region of contact is limited as in the armadillo, in which maternal blood sinuses are expanded to form intervillous spaces.

Animals↗
PubMed1985

Use of the term "trophoblast" for tissues in therian mammals.

Use of the term "trophoblast" in descriptions of therian (marsupial and eutherian) mammals has caused confusion because of misinterpretations of blastular homologies and because of imprecise application in functional versus ontogenetic-phylogenetic senses. Marsupials follow the plan of early development characteristic of noneutherian amniotes. Eutherians, in contrast, are unique in the early determination of presumptive embryonic versus extraembryonic cells through formation of inner cell mass versus trophoblastic (or trophectodermal) tissues, respectively. No cellular unit of the eutherian blastula is recognizable unequivocally as the homologue of a specific part of the protodermal marsupial blastula; progressive deletion of innovative but phylogenetically older ontogenetic steps probably figured importantly in the evolution of eutherian early embryogenesis. Because of marked differences in mode of formation and in cellular fates, homology of the blastocoel between marsupials and eutherians is questioned. It is suggested that use of the term "trophoblast" be restricted to eutherians in discussions of ontogenesis or phylogenesis, and be deemphasized in the functional sense (i.e., fetal-maternal exchanges) for marsupials, in favor of the more appropriate tissue terms of "choriovitelline" and "chorioallantoic" membranes. Integral to the origin of the eutherian style of embryogenesis was the evolution during Cretaceous time of neomorphic, extraembryonic tissues (i.e., trophoblast) having physiological properties that allowed the unique combination of intimate apposition of fetal and maternal tissues and circulatory systems, along with sustained, active morphogenesis. Marsupials have not achieved such a combination.

Animals↗
PubMed1992

Herpes simplex virus infection of cultured human term trophoblast.

Mononuclear trophoblast cells were isolated from term placentas of uncomplicated pregnancies, purified to homogeneity by negative immunomagnetic separation using monoclonal antibodies to the major histocompatibility complex, and challenged with herpes simplex virus (HSV). The cultures were highly susceptible to virus-induced cytopathic effect as evidenced by cytopathic alteration and inhibition of human chorionic gonadotropin (hCG) secretion. Both HSV I and II underwent a full replicative cycle in the trophoblast, although the production of progeny virus was 10-100 times less than that obtained with placental fibroblasts or choriocarcinoma cells. The permissiveness was independent of in vitro syncytial differentiation of the trophoblast. The results suggest that the trophoblast layer may be involved in intrauterine HSV infection.

Antibodies↗
PubMed2003

The pattern of expression of protease-activated receptors (PARs) during early trophoblast development.

Human fetal development depends on the ability of the embryo to gain access to the maternal circulation. Thus, specialized stem cells of the newly formed placenta, trophoblast, invade the uterus and its arterial network to establish an efficient feto-maternal molecular exchange. To accomplish this task, trophoblast differentiation during the first trimester of pregnancy involves cell proliferation, invasion, and extracellular matrix (ECM) remodelling. Trophoblast invasion shares many features with tumour cell invasion, with the distinction that it is strictly spatially and temporally controlled. We have previously demonstrated that PAR1, the first member of the protease-activated receptor (PAR) family, plays a central role in tumour cell invasion. In the present study we have examined the pattern of expression of PAR1 and other PAR family candidates during early human placental development. We show that PAR1 and PAR3 are highly and spatially expressed between the 7th and 10th weeks of gestation but not at the 12th week and thereafter. Likewise, high expression levels of PAR1 and PAR3 were observed in the cytotrophoblast cells of complete hydatidiform mole as compared to minimal levels in normal age-matched placenta. Together, our data suggest the involvement of PAR1 and PAR3 in restricted and unrestricted pathological trophoblast invasion.

Chorionic Villi↗
PubMed1991

Trophoblast-like cells sorted from peripheral maternal blood using flow cytometry: a multiparametric study involving transmission electron microscopy and fetal DNA amplification.

Three monoclonal antibodies (MAbs) against trophoblast (GB17, GB21, and GB25) and flow cytometry were used to sort trophoblast-like cells (TLCs) from peripheral blood of pregnant women. Sorted TLCs were processed for electron microscopy and fetal DNA amplification of the Y-specific sequences from mothers carrying male fetuses. At the ultra-structural level, most of the nucleated cells had the morphology of leucocytes, suggesting maternal contaminants, and we did not find the characteristic features of the free intervillous trophoblast cells. Nevertheless, polymerase chain reaction (PCR) analysis showed an amplification of Y-specific sequences in two out of three samples of sorted TLCs. These results suggest that besides the maternal leucocytes, sufficient trophoblast nucleated fetal cells can be obtained using cell enrichment by sorting. This sensitive method holds promise for non-invasive prenatal diagnosis of fetal sex and if sufficient Y(positive) nuclei are found, for the diagnosis of selected numerical chromosome abnormalities.

Antibodies, Monoclonal↗
PubMed2002

The role of hyperglycosylated hCG in trophoblast invasion and the prediction of subsequent pre-eclampsia.

OBJECTIVE: Hyperglycosylated hCG (HhCG) is the predominant form of chorionic gonadotrophin in states characterized by aggressive trophoblast invasion such as early pregnancy or choriocarcinoma. Pre-eclampsia may be the result of failed or inadequate trophoblast invasion. We investigated whether low levels of maternal urine HhCG levels would predict subsequent pre-eclampsia. STUDY DESIGN: Mid-trimester urine (14-21 weeks) was collected and frozen from non-hypertensive women undergoing genetic amniocentesis. Inclusion criteria were: normal singleton pregnancies without a prior history of pre-eclampsia, hypertension, diabetes or other vascular disorders. The specimens were subsequently thawed, and HhCG levels standardized to urine creatinine were measured. Maternal charts were reviewed after delivery to determine the development of pre-eclampsia. There were a total of 568 study subjects. RESULTS: Pre-eclampsia developed in 26 (4.6%) women. There was a significant correlation between low urine HhCG and subsequent pre-eclampsia (Mantel-Haenszel test of linear association: Chi-square 10.52, p=0.001). The mean HhCG level (ng/mg creatinine) was significantly greater in normals than in those destined to develop pre-eclampsia: 42.7 versus 20.3, p=0.002 (Mann-Whitney U-test). There was a progressive increase in the risk of subsequent pre-eclampsia as HhCG levels fell: HhCG < or =0.9 MoM RR (95% CI)=1.51 (1.15-1.98) compared with < or =0.1 MoM 10.42 (2.0-54.3). CONCLUSION: Low maternal mid-trimester urine HhCG predicted subsequent pre-eclampsia. This appears to support the view that pre-eclampsia results at least in part from poor trophoblast invasion. Thus, HhCG may play a role in trophoblast invasion and measurement of this in urine identifies women at high risk for developing pre-eclampsia.

Amniocentesis↗