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PubMed1995

Human trophoblast adhesion to matrix proteins: inhibition and signal transduction.

At the time of implantation, the extracellular matrix proteins laminin and fibronectin are abundant in the decidua and are distributed pericellularly around each individual stromal cell. First trimester human trophoblast expresses both laminin and fibronectin receptors, specifically the alpha 1 beta 1, alpha 5 beta 1, alpha 6 beta 1 and alpha 6 beta 4 integrin heterodimers. In this study we have demonstrated that in-vitro adhesion of first trimester human trophoblast to purified extracellular matrix proteins and to purified decidual stromal cell monolayers can be inhibited by monoclonal antibodies directed against appropriate integrin subunits and by synthetic peptides containing an arginine-glycine-aspartic acid sequence. Monoclonal antibodies (mAbs) to the alpha 5 and beta 1 integrin subunits and a synthetic peptide significantly inhibited adhesion to fibronectin. Binding of trophoblast to laminin was blocked with mAbs to the alpha 6 and beta 1 but not alpha 1 and beta 4 integrin subunits. Similarly, integrin-mediated adhesion to monolayers of decidual stromal cells could be blocked with mAbs to the alpha 5, alpha 6, beta 1 and beta 4 integrin subunits. Integrin-mediated signal transduction in normal and malignant trophoblast was investigated by Western blotting. A 115 kDa protein was the major tyrosine phosphorylated protein detected in trophoblast after binding to laminin or fibronectin. The profile of tyrosine phosphorylated proteins differed for malignant trophoblast.

3T3 Cells↗
PubMed1994

Trophoblasts circulating in maternal blood as candidates for prenatal genetic evaluation.

Trophoblasts have been detected in uterine venous blood, lung parenchyma and maternal blood in the first trimester. Their dilution within maternal leukocytes has been recently estimated to be 1:10(-6). The objectives of this study were to enrich peripheral maternal blood preparations for trophoblast cells, to isolate trophoblasts from the enriched preparation by highly specific markers and to assess fetal cell total number of chromosomal copies by fluorescence in-situ hybridization (FISH). Negative and positive selections for trophoblasts were performed. To assess the efficacy of the enrichment methods, a model mimicking the in-vivo conditions was established. Purified first trimester trophoblasts were prepared from first trimester placentas and were mixed with leukocytes from non-pregnant women in various concentrations. Magnetic beads coupled with antibodies to the common leukocyte antigen (CD45) or to antitrophoblast specific antigens (Trop1, Trop2 and GB25), were attached to peripheral maternal blood cells or to the prepared mixed cell populations. The expression of alpha human chorionic gonadotrophin (alpha HCG) or of human placental lactogen (HPL) by the remaining cells was examined by two means: (i) immunocytochemistry, using monoclonal antibodies against HPL and alpha HCG to stain fetal cells; (ii) reverse transcriptase polymerase chain reaction (RT-PCR), using specific primers for exons of the HPL or alpha HCG mRNAs. Results revealed that HPL- and alpha HCG-expressing cells could be identified in maternal blood only in very rare instances. On the other hand, expression of alpha HCG and HPL by only 100 purified first trimester trophoblasts artificially mixed with peripheral leukocytes at a ratio of 1:10(-5) could be identified by both immunocytochemistry and RT-PCR.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMed1993

Localization of transforming growth factor alpha in the human placenta and decidua: role in trophoblast growth.

Transforming growth factor alpha (TGF alpha) is an important growth regulatory molecule, the location and function of which at the human fetomaternal interface remain to be determined. The present study examined the presence of TGF alpha in the human placenta, decidua, and fetal membranes throughout gestation (from a total of 29 subjects) as well as its functional role in the proliferation of first trimester trophoblasts. The peptide was localized immunocytochemically with a monoclonal anti-TGF alpha antibody (Ab) (MF9) on paraffin-embedded tissues via the avidin-biotin complex-peroxidase technique with diaminobenzidine (DAB) as the chromogen. Omission or TGF alpha absorption of the primary Ab served as negative controls. Specific (cytoplasmic) staining was noted in typical stromal-type decidual cells, including cells of the decidua basalis and parietalis and chorionic decidua, throughout gestation. Villous trophoblast cells (syncytiotrophoblast and to a minor extent cytotrophoblast) at all gestational ages as well as extravillous cytotrophoblast cells (intermediate and cytotrophoblastic shell) also showed specific cytoplasmic staining. Chorionic trophoblasts showed variable staining, and little or no immunoreactivity was seen in the amniocytes. Second-passage first trimester human trophoblast cells (characterized by their expression of cytokeratin as well as other markers) were cultured in the presence of TGF alpha or neutralizing anti-TGF alpha Ab (TAb-1) or no additive for 18 h prior to exposure to 3H-TdR for 6 h to measure 3H-TdR uptake. TGF alpha (0-100 ng/ml) caused a dose-dependent stimulation of proliferation, reaching a near plateau at 6-100 ng/ml to slightly more than double the basal level. The presence of anti-TGF alpha Ab alone (25 micrograms/ml) did not significantly influence the proliferation of the cells, indicating the absence of significant endogenous TGF alpha in these cultures; however, the Ab was able to abolish the stimulatory function of exogenous TGF alpha. Exogenous TGF alpha also increased the number of trophoblast nuclei immunoreactive for proliferating cell nuclear antigen and reduced the incidence of multinucleate cells in culture. These results indicate that TGF alpha is present in the cells of the fetomaternal interface throughout human gestation and may function as a stimulator of trophoblastic growth in situ.

Cell Division↗
PubMed1995

Secretion of biologically active interferon tau by in vitro-derived bovine trophoblastic tissue.

Secretion of interferon tau (IFN tau) by trophoblastic tissue has been shown to be the first embryonic signal for pregnancy recognition. Therefore we tried to derive biologically active trophoblastic tissue by in vitro techniques. Since conventional in vitro conditions for bovine embryo development were not sufficient for long-term culture, we tested more complex culture conditions, including Ménézo B2 or Buffalo rat liver (BRL) cell-conditioned medium, for their ability to support proliferation and IFN tau secretion by in vitro-derived trophoblastic tissue. IFN tau activity was determined by using a biological assay based on the inhibition of the cytopathic effect of vesicular stomatitis virus on Madin-Darby bovine kidney cells. When cultures of individual hatched blastocysts were started in 60-microliters drops of BRL cell-conditioned medium, mean IFN tau secretion (antiviral units/ml/48 h) corresponded to 1200 on Day 11 and to 5000 on Day 13 (p < 0.01). To characterize trophoblast cell-specific secretions, the inner cell mass was removed from all embryos by microsurgery on Day 13. IFN tau secretion by trophoblastic tissue increased to mean levels of > 10(5) antiviral units/ml/48 h on Day 23m, stayed high for about 1 wk, and then slowly declined to levels below 10(3) antiviral U/ml/48 h. The specificity of the cytoprotective effect of IFN tau was tested by Western blot analysis and by immunoneutralization with use of a polyclonal antiserum specific to IFN tau. Our results demonstrate that viable trophoblastic tissue can be maintained entirely in vitro and secretes high amounts of IFN tau.

Animals↗
PubMed1999

Defective induction of the transcription factor interferon-stimulated gene factor-3 and interferon alpha insensitivity in human trophoblast cells.

During pregnancy, trophoblast cells of the placenta contact maternal immune cells and yet are protected from attack. One mechanism that may account for this is that trophoblasts show altered expression of major histocompatibility complex (MHC) antigens. The gene for human leukocyte antigen G (HLA-G), a nonclassical gene, is expressed at high levels in trophoblast. Unlike other MHC class I genes, the HLA-G gene lacks an interferon (IFN) response element. Moreover, we demonstrate here that IFN, which regulates classical MHC class I genes in other cell types, does not affect these genes in trophoblast, owing to inactivation of an IFNalpha signaling pathway. Trophoblast cells (JEG-3 and JAR) were found to be selectively refractory to IFN. Specifically, although IFNalpha induced the transcription factors STAT1, STAT2, and IFN regulatory factor-1, and a protective response against encephalomyocarditis virus, it failed to protect the cells from vesicular stomatitis virus, activate a transfected MHC class I gene promoter, and induce the transcription factor IFN-stimulated gene factor (ISGF)-3. The lack of ISGF3 DNA-binding activity apparently was due to diminished p48/ISGF3gamma subunit activity since ISGF3 DNA-binding activity and IFNalpha induction of MHC class I promoter activity were reconstituted by p48/ISGF3gamma supplementation. These data indicate that a specific IFN signaling pathway is inactive in JEG-3 trophoblast cells because of altered activity of p48/ISGF3gamma, and they suggest IFN insensitivity as a mechanism that may help promote feto-placental survival.

Choriocarcinoma↗
PubMed2002

Expression of fertilin and CD9 in bovine trophoblast and endometrium during implantation.

The superficial placentation of cattle involves the development of fetal binucleate cells that arise from the chorion and migrate between adjacent cell tight junctions to fuse with maternal epithelium. Thus, the temporal and spatial patterns of expression of the cell migration, adhesion, and fusion molecules fertilin and CD9 were investigated in bovine trophoblast and endometrium. Bovine fertilin alpha and fertilin beta messenger RNA sequences were amplified by reverse transcriptase-polymerase chain reaction in testis (positive control), peri-implantation (Days 18, 19, and 21), and postimplantation (Days 35-40) trophoblast RNA, but not in caruncular endometrium (Day 40). Northern blot analysis indicated that the transcript hybridizing to fertilin alpha in trophoblast RNA was approximately 4.0 kilobases (kb), whereas in testis, 2 transcripts of approximately 3.3 and 3.8 kb were indicated. The transcript hybridizing to the fertilin beta probe was also larger in trophoblast than in testis ( approximately 3.8 vs. 2.4 kb, respectively). In situ hybridization revealed that fertilin beta mRNA was expressed by trophoblast cells, including binucleate cells. Immunohistochemical study of CD9, a member of the transmembrane-4-superfamily which is thought to be involved in sperm-egg fusion, showed that CD9 was present on the apical surface of uterine epithelium and in a subpopulation of binucleate cells of the trophoblast. Immunoprecipitation followed by Western blot analysis showed association between CD9 and integrin alpha3 in endometrium. The results support the hypothesis that fertilin and CD9 are involved in bovine binucleate cell migration and fusion.

ADAM Proteins↗
PubMed1998

Sustained hyperglycemia in vitro down-regulates the GLUT1 glucose transport system of cultured human term placental trophoblast: a mechanism to protect fetal development?

The trophoblast of human placenta is directly exposed to the maternal circulation. It forms the main barrier to maternal-fetal glucose transport. The present study investigated the effect of sustained hyperglycemia in vitro on the glucose transport system of these cells. Trophoblasts isolated from term placentas and immunopurified were cultured for 24, 48, and 96 h in DMEM containing either 5.5 (normoglycemia) or 25 mmol/l D-glucose (hyperglycemia), respectively. Initial uptake of glucose was measured using 3-O-[14C]methyl-D-glucose. Kinetic parameters were calculated as K(M) = 73 mmol/l and Vmax = 29 fmol s(-1) per trophoblast cell. Uptake rates of cells cultured under hyperglycemic conditions did not differ at exogenous D-glucose concentrations in the physiological range (1, 5.5, 10, and 15 mmol/l), but were significantly decreased by 25% (P<0.05) at diabetes-like concentrations (20 and 25 mmol/l) as compared to normoglycemic conditions. This effect was due to a decrease in Vmax (-50%), whereas K(M) remained virtually unaffected. GLUT1 mRNA levels were lower by 50% (P<0.05; Northern blotting) and GLUT1 protein was reduced by 16% (P<0.05; Western blotting) in trophoblast cells cultured under hyperglycemic vs. normoglycemic conditions. We conclude that prolonged hyperglycemia in vitro reduces trophoblast glucose uptake at substrate concentrations corresponding to blood levels of poorly controlled diabetic gravidas. This effect is due to diminished GLUT1 mRNA and protein expression in the trophoblast.

3-O-Methylglucose↗
PubMed1993

Endothelin-1 binding sites and immunoreactivity in the cultured human placental trophoblast: evidence for an autocrine and paracrine role for endothelin-1.

In human placenta, endothelin (ET) could derive from maternal, fetal, and/or endogenous sources. Therefore, localization of ET-1 was investigated by immunohistochemistry in human term placenta and in cultured trophoblasts. In sections of placenta, ET-1 immunoreactivity (ET-1 IR) was specifically detected in the endothelium of the vessels and in the syncytiotrophoblasts of the villi. ET-1 IR was also detected in the decidual cells and in the extravillous cytotrophoblasts of the basal plate. The extravillous cytotrophoblasts of the chorionic plate and of the placental septa also exhibited strong ET-1 IR. For trophoblast culture, cytotrophoblastic cells were obtained from placental villi by trypsin-DNAse dispersion, further purified on a Percoll gradient, and enriched by employing a monoclonal anti-HLA class I antibody. After different periods of culture of purified cytotrophoblastic cells (1-5 days), ET-1 IR was observed in 95% of cells: cytotrophoblastic cells, trophoblast aggregates, and syncytiotrophoblasts. The presence of ET-1,2 immunoreactivity (ET-1,2 IR) in the culture media was demonstrated by radioimmunoassay. A uniform daily production of the peptide was observed over at least 5 days (approximately 50 fmol/10(6) cells/24 h). Furthermore, trophoblastic cells that had been cultured for 5 days contained significant amounts of ET-1,2 IR (24 fmol/10(6) cells). These results suggest a trophoblastic origin for ET-1 and support the hypothesis of a paracrine and autocrine action of the peptide in the physiology of the trophoblast and placenta.

Adult↗
PubMed1994

Correlation of uterine hemodynamics with chemotherapy response in gestational trophoblastic tumors.

OBJECTIVE: To assess the uterine hemodynamics in gestational trophoblastic tumors and to correlate them with response to chemotherapy. METHODS: Using transvaginal color Doppler ultrasound, we measured the peak systolic velocity and the resistance index (RI) of the uterine arteries in 23 women with gestational trophoblastic tumors before each course of chemotherapy. Fifty-five nonpregnant women and another 15 women who had uneventful molar evacuation were enrolled as controls. Two-tailed Student t test was used for statistical analysis. RESULTS: A hyperdynamic uterine circulation was noticed at diagnosis in all gestational trophoblastic tumors, manifested as higher peak systolic velocity (mean +/- standard deviation 57.5 +/- 20.4 cm/second) of the uterine arteries compared to nonpregnant (28.3 +/- 3.41 cm/second; P < .0001) and uneventful post-mole uteri (26.8 +/- 3.08 cm/second; P < .0001). The RI values of the uterine arteries in gestational trophoblastic tumors at diagnosis ranged from 0.21-0.80. However, the mean value (0.56 +/- 0.19) was lower than those of nonpregnant (0.80 +/- 0.05; P < .0001) and post-mole uteri (0.75 +/- 0.06; P < .0001). A higher pre-treatment uterine artery RI (mean 0.71 +/- 0.09) was noted in ten patients with gestational trophoblastic tumors requiring fewer than five courses of chemotherapy, compared with the mean in 13 patients requiring longer courses of treatment (0.47 +/- 0.14; P < .0001). There was a marked decrease of peak systolic velocity during the first three courses of treatment in the former group (54.2 to 23.6 cm/second; P < .001), in contrast to no change in the latter group (60.1 to 60.5 cm/second). CONCLUSION: Uterine hemodynamic characteristics assessed by color Doppler ultrasound might predict and monitor the response to chemotherapy in gestational trophoblastic tumors.

Adult↗
PubMed2005

Osteopontin expression in gestational trophoblastic diseases: correlation with expression of the adhesion molecule, CEACAM1.

The human placenta is a complex tissue with multiple endocrine and nutritional functions and a unique capacity for rapid proliferation but tightly controlled invasion, differentiating it from malignant tumors. Osteopontin (OPN) is a glycoprotein of the extracellular matrix, which has been shown to mediate cellular migration and invasion and to contribute to tumorigenesis in several types of cancers. OPN also could be implicated in regulating implantation and placentation by promoting cellular migration and invasion in a placenta-specific fashion. We could demonstrate the expression pattern of OPN in the normal human placenta in which it is localized in the extravillous (intermediate) trophoblast and the villous cytotrophoblast. CEACAM1 is an adhesion molecule, which we have recently found to be expressed at the maternal-fetal interface of the normal placenta with a localization to the extravillous (invasive) trophoblast and in gestational trophoblastic disease (GTD) and also to be potentially implicated in trophoblast invasion and tumorigenesis. Both OPN and CEACAM1 have been shown to interact with integrin beta3. The purpose of this study was to investigate the expression pattern of OPN in GTD and to correlate it with the expression of CEACAM1. To analyze the expression of OPN, we performed immunohistochemistry on a total of 27 cases of GTD, including 21 hydatidiform moles and 6 choriocarcinomas, which had previously been characterized with respect to their CEACAM1 expression. Hydatidiform moles showed a positivity for OPN in villous cytotrophoblast and in the trophoblast proliferations on the villous surface. The strongest OPN expression could be observed in the choriocarcinomas with a heterogenous OPN expression pattern. CEACAM1 had shown similar results and was found to be expressed in choriocarcinoma. The expression pattern of osteopontin in gestational trophoblastic diseases indicates that it might play a role in the pathogenesis of GTD (possibly as a functional complex with CEACAM1 and integrin beta3) and might be useful as an additional diagnostic marker for such lesions.

Antigens, CD↗
PubMed1979

Oncofoetal antigens of human trophoblast.

Rabbits immunized with human trophoblast cell membranes produced antibodies that were detected, by immunofluorescence, to react with normal human tissues, and, by complement-mediated cytotoxicity, with several transformed human cell lines. Absorption with trophoblast abolished all of these reactions, whereas multiple absorptions with lymphocytes, liver or kidney failed to remove reactivity with either trophoblast or certain transformed cells. To further identify the antigens responsible for these antibodies, rabbits were immunized with a chromatographed fraction of deoxycholate-solubilzed membranes prepared from KCl-extracted, ultracentrifuge-prepared trophoblast microvilli. The resultant IgG antibody reacted specifically with syncytiotrophoblastic membranes in sections of human placentae, in addition to recognizing the membranes of viable Chang liver, AV3, HEp-2, Sw/156 (kidney) and Sw/527 (breast) cells. That normal tissues, baboon or monkey placentae, and HeLa or Daudi cell lines did not react with this antibody, indicates the presence of species- and organ-specific antigens in human trophoblast, as well as the existence of trophoblast cross-reactive antigens on some transformed cells. The selective localization of these antigens at the interface of the materno-foetal graft suggests that they function biologically in the host-parasite relation of human pregnancy; their appearance on many transformed cells implies a similar function in the host-parasite relation of some human cancers.

Animals↗
PubMed2006

Human endogenous retrovirus-W envelope (syncytin) is expressed in both villous and extravillous trophoblast populations.

The placenta is unique amongst normal tissues in transcribing numerous different human endogenous retroviruses at high levels. In this study, RT-PCR and immunohistochemistry were used to investigate the expression of syncytin in human trophoblast. Syncytin transcripts were found in first-trimester trophoblast cells with both villous and extravillous phenotypes and also in the JAR and JEG-3 choriocarcinoma cell lines. Syncytin protein was detected in villous trophoblast and in all extravillous trophoblast subpopulations of first- and second-trimester placental tissues. It was also present in ectopic trophoblast from tubal implantations. This study confirms that syncytin is expressed widely by a variety of normal human trophoblast populations, as well as choriocarcinoma cell lines.

Cell Line, Tumor↗
PubMed2001

Diethylstilbestrol regulates trophoblast stem cell differentiation as a ligand of orphan nuclear receptor ERR beta.

The orphan nuclear receptor ERR beta is expressed in undifferentiated trophoblast stem cell lines and extraembryonic ectoderm, and genetic ablation of ERR beta results in abnormal trophoblast proliferation and precocious differentiation toward the giant cell lineage. Here, we show that the synthetic estrogen diethylstilbestrol (DES) promotes coactivator release from ERR beta and inhibits its transcriptional activity. Strikingly, treatment of trophoblast stem cells with DES led to their differentiation toward the polyploid giant cell lineage. In addition, DES-treated pregnant mice exhibited abnormal early placenta development associated with an overabundance of trophoblast giant cells and an absence of diploid trophoblast. These results define a novel pathway for DES action and provide evidence for steroidlike control of trophoblast development.

Animals↗
PubMed2004

p57(KIP2) immunohistochemical staining of gestational trophoblastic tumours does not identify the type of the causative pregnancy.

AIM: To determine whether immunohistochemical staining for p57(KIP2), the product of the maternally expressed gene CDKN1C, can be used to differentiate between gestational trophoblastic tumours arising from a complete hydatidiform mole and those originating from non-molar pregnancies. METHODS: The immunohistochemical expression of p57(KIP2) was investigated in 23 cases of choriocarcinoma and 17 placental site trophoblastic tumours. Fourteen of the tumours examined were shown by DNA analysis to have arisen from complete hydatidiform moles and 26 from non-molar pregnancies. RESULTS: Five of 11 (45%) post-complete hydatidiform mole choriocarcinomas and two of three (67%) post-complete hydatidiform mole placental site trophoblastic tumours were found to be p57(KIP2)+ and showed similar immunostaining characteristics to tumours that developed from non-molar pregnancies. Although there was a statistically significant reduction in the proportion of cases showing positive p57(KIP2) staining in post-complete hydatidiform mole tumours compared with those originating in non-molar pregnancies [proportion difference 0.35 [95% confidence interval (CI) 0.05, 0.61], P = 0.02], immunostaining did not provide diagnostically useful information to differentiate between these tumours in clinical practice. There was no significant difference between the extent of staining in choriocarcinoma versus placental site trophoblastic tumours [proportion difference 0.17 (95% CI - 12, 42), P = 0.19]. The majority of both types of gestational trophoblastic tumour were positive for the presence of the p57(KIP2) protein irrespective of their genetic origin. CONCLUSION: Immunostaining for p57(KIP2) fails to discriminate between gestational trophoblastic tumours that have arisen from complete hydatidiform moles and those that have originated from other types of pregnancy.

Adult↗
PubMed1994

Invasion and replication of Brucella abortus in three different trophoblastic cell lines.

This study was performed to compare the replication of the pathogenic strain Brucella abortus 2308 in three trophoblastic cell lines derived bovine placentas at different gestational stages. The trophoblastic cell lines were obtained from a 13-15 day embryo, from 5-month placentomal tissue and from an 8-month extra-placentomal portion of the placenta. The infection rate was similar in all cell lines at 4 h. Colony-forming Units were counted at 4, 8, 12, 24 and 30 h post-inoculation. At 12, 16, 24 and 30 h B. abortus rapidly replicated within the 5-month and 8-month trophoblastic cell lines, but grew slowly within trophoblastic cells derived from embryonic tissue. Electron microscopic studies consistently showed clusters of B. abortus in trophoblastic cells derived from 5- and 8-month placentas, while few cells of the embryonic line were infected and these contained only 1-2 bacteria per cell. It was concluded that B. abortus can infect trophoblastic cells throughout the gestational period but bacterial multiplication does not occur in these cells before middle or late gestation.

Animals↗
PubMed1994

Persistent gestational trophoblastic tumour with partial hydatidiform mole as the antecedent pregnancy.

OBJECTIVE: A 16 year review of persistent gestational trophoblastic tumour when the antecedent pregnancy was a partial hydatidiform mole. DESIGN: Cases of persistent gestational trophoblastic tumour with partial hydatidiform mole as the antecedent pregnancy were reviewed for the period 1976 to 1992. DNA ploidy was analysed by flow cytometry. SETTING: A University Hospital which is a reference centre for gestational trophoblastic tumour. SUBJECTS: The case notes of 207 women with persistent gestational trophoblastic tumour were reviewed. MAIN OUTCOME MEASURES: A rise (or failure to fall) of beta hCG titre, or sign of metastasis. RESULTS: Six (2.9%) women had partial hydatidiform mole as the antecedent pregnancy and all were initially judged to be low risk. However, two developed pulmonary metastasis; one woman developed persistent gestational trophoblastic tumour shortly after a hysterotomy, and none developed choriocarcinoma. The geometric mean of serum beta hCG concentrations at the initiation of chemotherapy was 868 mIU/ml (95% CI 114-1524). Of the six women, one achieved remission after total abdominal hysterectomy, and five after chemotherapy. The mean interval from starting treatment to remission was 68 days (95% CI 27.9-108.0). The initial beta hCG titre and interval were not statistically different from those found in cases of persistent gestational trophoblastic tumour when the antecedent pregnancy was not partial hydatidiform mole. Of the six, the DNA content was triploid in three and diploid in two. One of the two diploid cases required multiple courses of chemotherapy to achieve remission. CONCLUSION: Partial hydatidiform mole can have malignant sequelae and can develop very soon after treatment. Its DNA content can be either diploid or triploid, the lungs being the most common site of metastasis. After evacuation of partial hydatidiform mole, immediate chest X-ray and regular follow up of the serum beta hCG level is necessary.

Adult↗
PubMed1987

Effects of cadmium on preimplantation and early postimplantation mouse embryos in vitro with special reference to their trophoblastic invasiveness.

Cadmium chloride, at concentrations of 0.5 or 1 microgram/ml medium, did not affect the trophoblastic invasiveness of mouse embryos treated for 24 hours at 4-cell and morula stages. At higher concentrations of 5 or 10 micrograms/ml medium, most treated embryos in vitro underwent degeneration while a few survivors formed trophoblastic outgrowths with variable areas. Cadmium chloride, at a low concentration of 0.5 microgram/ml medium presented continuously to blastocysts after attachment in vitro, has significantly retarded the trophoblastic outgrowth areas and reduced the number of trophoblastic giant-cell nuclei, though the spreading blastocysts appeared morphologically normal. At higher concentrations of 1 or 5 micrograms/ml medium, cytoplasmic disintegration and detachment of trophoblasts were observed. It is suggested that cadmium may interfere with the cell division and/or the transformation of trophectoderm cells into giant cells, resulting in the retardation of the trophoblastic outgrowths.

Animals↗
PubMed1995

The effect of zidovudine and 2'3'-dideoxyinosine on human trophoblast in culture.

Trophoblast from term and first trimester placenta, maintained in culture, were exposed to 20 mumoles/l zidovudine or 2'3'dideoxyinosine. Several indices of function were measured and compared to control trophoblast in parallel culture. The results from individual placentas were examined by Student's t-test and cumulative results by ANOVA. Neither zidovudine or 2'3'-dideoxyinosine had statistically significant effects on the function of term trophoblast, following a 48 hr exposure to the drug as indicated by hCG secretion, protein synthesis and glucose consumption. In one of five placentas exposed to zidovudine, progesterone secretion was reduced as compared to its control but remained in the high range. Zidovudine had no significant effect on cultured trophoblast isolated from first trimester placenta even after prolonged exposure to the drug for eleven days. Both term and first trimester trophoblast in culture tolerate prolonged exposure to high concentrations of zidovudine or 2'3'-dideoxyinosine. Human trophoblast in culture provides a safe in vitro model for the screening of drugs intended for use during pregnancy.

Analysis of Variance↗