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At least 1,171 records · Page 65Linked to original sources
PubMed1994

Metabolism of 3'-azido-3'-deoxythymidine (AZT) in human placental trophoblasts and Hofbauer cells.

3'-Azido-3'-deoxythymidine (AZT) is currently under clinical investigation to assess its potential to inhibit maternal-fetal HIV transmission. To determine the activation of AZT to its phosphorylated metabolites by placental cells, we characterized the intracellular phosphorylation of AZT in two major cell types of the placenta, namely trophoblasts and Hofbauer cells. Although phosphorylation of AZT in trophoblast and Hofbauer cells is 50- to 100-fold lower than that in human lymphocytic cell lines or activated lymphocytes, both cell types are capable of activating AZT to AZT triphosphate (AZTTP) at a level comparable to that of resting lymphocytes. We found that AZT monophosphate (AZTMP) was the major phosphorylated AZT metabolite, while AZT diphosphate (AZTDP) and AZTTP constituted less than 4% of the intracellular phosphorylated AZT pool. This result was independent of AZT concentration and exposure time in both types of placental cells. The rate-limiting step in the conversion of AZT to AZTTP was determined to be thymidylate kinase-catalyzed conversion of AZTMP to AZTDP. Trophoblasts and Hofbauer cells exhibited different time-course and concentration-dependent profiles of intracellular AZT phosphorylation, suggesting that these two placental cells may have anabolic or catabolic enzymes of different composition or efficiency. AZTTP decayed in both trophoblasts and Hofbauer cells with a half-life of 4-6 hr. These results should be useful in rationally designing AZT dosage regimens to treat HIV-infected women for prevention of maternal-fetal HIV transmission.

Cell Line↗
PubMed1990

Human trophoblast and JEG choriocarcinoma cells are sensitive to lysis by IL-2-stimulated decidual NK cells.

Freshly isolated decidual large granular lymphocytes (LGL) show natural killer (NK) activity against K562 cells but not against normal human trophoblast. We now show that these decidual LGL proliferate in vitro in response to recombinant interleukin-2 (rIL-2) and that these rIL-2-stimulated cells acquire a broad cytolytic potential that is characteristic of lymphokine-activated killer (LAK) cells. Both fetal fibroblasts and JEG-3 choriocarcinoma cells are resistant to lysis by freshly isolated decidual effectors but are readily killed by IL-2-stimulated decidual LGL. The ability to kill these target cells is acquired after only 18 hr exposure to rIL-2. rIL-2-activated decidual LGL also kill cultured normal trophoblast cells but much lower levels of cytolysis were seen even after the effectors had been stimulated with rIL-2 for 4-6 days. The preferential killing of malignant over normal human trophoblast cells raises questions about the potential role of IL-2-activated decidual LGL in the control of unduly invasive or malignant trophoblast populations in vivo.

Antigens, CD↗
PubMed1990

The role of murine cell surface galactosyltransferase in trophoblast: laminin interactions in vitro.

Implantation of the mouse embryo involves the invasion of the secondary trophoblast giant cells of the ectoplacental cone (EPC) into the uterine decidua. The mechanisms of this event are poorly understood. The putative substrate molecules found in the decidua which could support trophoblast invasion include laminin, fibronectin, and collagen type IV. EPCs dissected from Day 7.5 embryos were cultured on all three matrices. Galactosyltransferase (GalTase) was localized by immunolabeling on trophoblast cell surfaces when grown on laminin but not the other matrices. Perturbations of the enzyme:substrate complex with alpha-lactalbumin, uridine diphosphogalactose, anti-GalTase, and pregalactosylation of the matrix did not affect rates of EPC attachment. However, decreased rates of migration or altered morphologies of spreading cells were observed. Laminin, and not fibronectin or collagen type IV, could be galactosylated with both exogenous GalTase or EPC outgrowths. Digests of galactosylated laminin produced a glycoconjugate substrate with a molecular weight of less than 10K. The results suggest that invasive secondary trophoblast cells possess a GalTase-mediated migration system that is functional on laminin.

Animals↗
PubMed1986

Induction of metallothionein in a human trophoblast cell line by cadmium and zinc.

The induction of metallothionein (MT) in a cell line derived from a malignant trophoblastic tumor (JAr cells) was demonstrated using the Cd/heme radioassay following exposure to Cd or Zn. Cd at an optimal concentration of 1 microM produced a 30-fold increase in MT following a 24 hr incubation. Induction by Cd was both time and dose dependent, with a significant increase in MT noted as early as 3 hr, with levels continuing to increase up to 24 hr. Zn was also quite effective in inducing MT synthesis in this cell line. Exposure to 80 microM Zn for 24 hr produced a 70-fold increase in MT. Although Cd was a more potent inducer of MT, exposure to Zn resulted in a greater magnitude of induction. The magnitude of MT induction in JAr cells was much greater than that seen in cultured trophoblasts from term chorion laeve. The degree of induction seen in this cell line makes it an interesting model for the study of MT's role in trophoblast function. MT induction in trophoblasts may reflect a protective mechanism against heavy metal toxicity and/or an integral aspect of normal zinc homeostasis.

Cadmium↗
PubMedDate not supplied

Signal for term parturition is of trophoblast and therefore of fetal origin.

Up to now we know, that cytokines are key intermediates in the mechanisms, responsible for intrauterine activation in case of intra amniotic infection. The aim of our study was to investigate the role of cytokine- and prostaglandin production in normal term labor. Release of Il-6, Il-1 beta, TNF-alpha, PGE2, PGF2 alpha, was monitored in vaginal secretions originating from uterine cavity, cervix and vagina during normal course of labor. Cells from fetal membranes, decidua and villous trophoblast, obtained from placentas of patients after spontaneous delivery (n = 12), or without labor, after elective cesarean section (n = 12), were cultured, in order to identify cytokine and prostaglandin producing cells. In all cases, term labor and parturition was associated with strongly elevated cytokine- and prostaglandin concentrations in cervical secretions. Cell culture experiments clearly demonstrated, that cells from villous trophoblast, cultured after spontaneous delivery produced significantly more cytokines and prostaglandins than cells form villous trophoblast, cultured after elective cesarean section. Cells from fetal membranes also produced more Il-6 and PGE2 after labor. In contrast to that, cells from decidua produced similar amounts of cytokines and prostaglandins before and after spontaneous term labor. Therefore we conclude, that the signal for term labor and delivery is of trophoblast and so of fetal origin.

Amniotic Fluid↗
PubMed1983

Pelvic ultrasonography and the management of gestational trophoblastic disease.

Pelvic ultrasonography was performed in 33 patients with persistent gestational trophoblastic disease (GTD) and the sonographic findings were compared in all patients with laparoscopic findings and histologic material from endometrial curettage and/or hysterectomy. Ultrasonography indicated trophoblastic uterine involvement in 17 patients (51.5%) and the ultrasound interpretation was histologically confirmed in all 17 patients by endometrial curettage and/or hysterectomy. Among the 16 patients in whom the uterus appeared normal by ultrasound, endometrial curettings demonstrated scanty fragments of trophoblastic tumor in 6 patients (37.5%). Furthermore, in all 16 patients in whom the uterus appeared normal by ultrasound, laparoscopy also revealed no uterine abnormalities. Ultrasonography appears to be accurate in detecting extensive trophoblastic uterine involvement and helpful in identifying resistant uterine foci. Pelvic ultrasonography should be an integral part of the pretreatment assessment of patients with persistent GTD.

Adolescent↗
PubMed1983

A quantitative study of nuclear DNA of trophoblastic cells: proliferation kinetics.

The nuclear DNA contents of labeled and unlabeled nuclei of trophoblastic cells of 8 normal pregnancies, 2 missed abortions, and 14 cases of trophoblastic diseases were measured by Feulgen-DNA cytofluorometry combined with autoradiography. Syncytiotroblasts were rarely labeled and were considered to be inactive with regard to cell proliferation. Most of the labeled cells were cytotrophoblasts. The predominantly labeled cells ranged between 2 and 4C in cases of normal pregnancy and missed abortion, and a shift to a higher ploidy was seen in the more grave trophoblastic disease. From the point of cellular proliferation kinetics of trophoblastic cells, it is presumed that the cells in cases of normal pregnancy and type I hydatidiform mole are in the 2C cell cycle and in type II hydatidiform mole and in invasive mole there are heterogeneous cell populations, most of which are in the 2C cell cycle while the remaining are undergoing polyploidization or aneuploidization. In choriocarcinoma, the cells are not in the 2C cell cycle and also are probably undergoing polyploidization or aneuploidization in the hyper-4C area.

Abortion, Missed↗
PubMed1989

Eclampsia as a possible risk factor for persistent trophoblastic disease.

Twenty cases of hydatidiform mole complicated by eclampsia with adequate postevacuation follow-up are identified in a review of the literature since 1866. The clinical presentation of each of these patients is reviewed with particular attention to the existence of known risk factors for persistent trophoblastic disease. After excluding 3 women with coexisting fetus and 2 others who were treated initially with a total abdominal hysterectomy, it was discovered that 14 of the remaining 15 women developed persistent trophoblastic disease. This frequency of persistent trophoblastic disease is greater than can be explained based on previously described risk factors and suggests that the occurrence of eclampsia may be an independent risk factor for persistent trophoblastic disease.

Adult↗
PubMedDate not supplied

HLA expression by trophoblast of invasive moles.

HLA expression by the trophoblast in invasive hydatidiform mole was analysed by immunoperoxidase staining. In the invading villi of an invasive mole, villous trophoblast, both syncytiotrophoblast and cytotrophoblast, failed to show a positive reaction for HLA-A, -B and -C and HLA-DR. By contrast, extravillous trophoblast showed an intense reaction for HLA-A, -B and -C. The distribution of HLA antigens in the invading villi was the same as in the non-invading villi, and the antigens were also indistinguishable from those noted in non-invasive hydatidiform moles. The histopathology of invasive mole may suggest that it is a malignant neoplasm. This immunohistochemical study, however, lends support to the current view that invasive mole is a variant of a benign hydatidiform mole rather than a form of malignant trophoblastic disease.

Female↗
PubMedDate not supplied

Placenta accreta: an immunohistological study of trophoblast populations.

Trophoblast populations in four cases of placenta accreta were characterized using antibodies directed against cell membrane antigens, placental hormonal products and low-molecular-weight cytokeratins in standard immunoperoxidase techniques. The results obtained with antibody to syncytiotrophoblast membrane (rabbit anti-StMPM), antibody to an epithelial membrane antigen (HMFGI) and a cytokeratin marker (CAM 5.2) appeared identical to those reported for normal term placental tissues. Similarly the localization of human placental lactogen (hPL), human chorionic gonadotrophin (hCG) and pregnancy-specific beta 1-glycoprotein (SP1) within trophoblast populations in placenta accreta was identical to their reported distribution in term placenta. However, increased reactivity at the villous-maternal junction was demonstrated with NDOGI, an antibody raised against term syncytiotrophoblast membrane and directed against hyaluronic acid. NDOGI reactivity at this site is normally maximal during early placental development and is virtually absent in the third trimester. The results suggest that placenta accreta does not arise through excessive trophoblast invasiveness or proliferation and the absence of decidua is of more importance in the pathogenesis. Trophoblast may regulate its development at an unfavourable intramyometrial implantation site by the production of hyaluronic acid.

Antigens, Surface↗
PubMedDate not supplied

Human trophoblast cells cultured in modified medium and supported by extracellular matrix.

This paper describes a culture procedure which consistently yields 80 to 90 per cent trophoblast from human first-trimester placentae. The trophoblast cells are selected and maintained but there is no increase in proliferation. The cultured cells are found to resemble extravillous rather than villous trophoblast in their immunocytochemical characteristics. This technique provides a means of obtaining human trophoblast cells with a sufficient degree of homogeneity and viability to be used for in vitro experiments.

Antibodies, Monoclonal↗
PubMed1980

Immunological parameters in gestational trophoblastic neoplasia.

Immunological function were studied in 22 patients with hydatidiform mole and 29 patients with malignant trophoblastic disease before and after treatment; normal pregnant and post-pregnant women served as controls. The only significant abnormality in hydatidiform mole was a low granulocyte chemotaxis before evacuation. In malignant trophoblastic disease the total lymphocyte counts, T-cell counts. B-cell counts, lymphocyte responses to mitogens and serum IgA levels were significantly lower than in normal women 6 wk after pregnancy. In those who responded to chemotherapy, these indices rose to the levels of post-pregnancy controls. An 'immune profile score' based on these indices was found to be a useful prognostic index. All patients with hydatidiform mole who had a score of 7 or less developed malignant trophoblastic disease, while the two patients with malignant trophoblastic disease who died had the lowest scores of the series.

Adolescent↗
PubMed1980

Immunoferritin localisation of antigens of the microvillous membrane of human trophoblast.

Antiserum raised to purified plasma membranes of the human trophoblast (TrPM) was used in an indirect immunoferritin method to investigate the expression of specific membrane antigens in explants of human trophoblast and in cultured cells. Ferritin deposits occurred in discrete regions on the microvillous membrane of the syncytiotrophoblast, and these deposits also occurred in coated areas of the membrane. Discrete staining was also seen in cultured trophoblast cells and HeLa cells. Human amnion cells had a strong positive reaction for the TrPM antigens, but foetal skin cells and HEp-2 (larynx carcinoma) cells were negative. TrPM antigens appear to be highly specific for trophoblast and amnion, only being found otherwise as a result of placental genomic re-expression in neoplasia.

Antigens, Surface↗
PubMed1987

Class I major histocompatibility complex antigen expression on early murine trophoblast and its induction by lymphokines in vitro. II. The role of gamma interferon in the responses of primary and secondary giant cells.

The induction of paternal Class I and II MHC antigens by crude lymphokine preparations or purified recombinant gamma interferon was investigated on (C57BL/6J X CBA/H)F1 primary and secondary trophoblast giant cell outgrowths from 3.5-day post-coital (pc) blastocyst and 7.5-day pc ectoplacental cone preparations, respectively, using sensitive immunogold labelling techniques and electron microscopy. Class I MHC (but not Class II) antigens could readily be induced on secondary trophoblast giant cells, by incubation in vitro with gamma interferon for 40 h. However, repeated attempts to induce detectable MHC antigens on primary trophoblast giant cells failed. Mock-treated (C57BL/6J X CBA/H)F1 secondary trophoblast giant cell control preparations failed to express detectable MHC antigens. These findings suggest that, at the time of implantation, there is a time window during which MHC antigens are neither expressed constitutively nor are inducible by soluble factors which normally modulate cell surface MHC antigen concentration.

Animals↗
PubMed1987

Monoclonal antibodies to human trophoblast and sperm antigens: report of two WHO-sponsored workshops, June 30, 1986--Toronto, Canada.

Two WHO-sponsored workshops were recently held to obtain a consensus view from researchers active in the field of reproductive immunology on the current status of the application of monoclonal antibodies to studies of molecular events underlying reproduction and to determine the feasibility of using this approach to identify trophoblast- or sperm-specific antigens that might represent suitable candidates for the development of antifertility vaccines. A total of 66 mouse monoclonal antibodies reacting with human sperm and 45 monoclonal antibodies reacting with human trophoblast membrane components were submitted by 29 laboratories. These were evaluated in coded form by 42 laboratories with the appropriate expertise in biochemistry, immunohistology and tests of reproductive cell function. The majority of both anti-sperm and anti-trophoblast monoclonal antibodies cross-reacted with cellular elements in non-reproductive tissues. However, at least five monoclonal antibodies (two anti-trophoblast and three anti-sperm) appeared to demonstrate sufficient specificity to warrant further investigation as reagents for the identification of antifertility vaccine candidates.

Antibodies, Monoclonal↗
PubMed1988

Antibodies to trophoblast in normal pregnant and secondary aborting women.

Enzyme-linked immunosorbent assays (ELISA) with the use of chorionic villous plasma membranes prepared from first trimester and term placentae were employed to detect antibodies to trophoblast in normal primigravid women. Normal pregnant women were found to produce IgG antibodies to trophoblast. These antibodies could be eluted from first trimester placentae. This antibody response was observed in the first trimester and gradually decreased as pregnancy progressed. IgM antibody responses were observed only in the third trimester. Antibodies in some primigravid women and secondary recurrent aborters showed allotypic reactivity with individual trophoblast membranes. This finding was confirmed by immunoblotting experiments in which antibodies from some normal pregnant women were shown to recognize the same trophoblast antigens as those recognized by antibodies from secondary recurrent spontaneous aborters.

Abortion, Habitual↗
PubMed1988

Expression of the proliferation markers Ki67 and transferrin receptor by human trophoblast populations.

Immunohistochemical techniques were used to investigate the expression of proliferation markers (Ki67 and transferrin receptor) by fetal trophoblast in normal human pregnancy. In placental villous tissue, transferrin receptor was detected not only on the apical syncytiotrophoblastic membrane but also on the proximal portion of cytotrophoblast columns, an area of high cellular proliferative activity. The majority of cells in cytotrophoblast columns and shell showed nuclear reactivity with Ki67. Villous syncytiotrophoblast was uniformly unreactive with Ki67 but a proportion of the underlying cytotrophoblast was Ki67-positive throughout pregnancy. Occasional Ki67-positive trophoblast cells were identified within chorion laeve at term. In contrast, interstitial and endovascular extravillous trophoblast in maternal uterine decidual tissue failed to label with either proliferation marker. Thus, chorionic villous cytotrophoblast and extravillous trophoblast in the chorion laeve appear to retain their proliferative capacity into late pregnancy. Cytotrophoblast columns represent a zone of cellular proliferation which may be dependent on transferrin.

Biomarkers↗
PubMed1989

Effects of baboon chorionic gonadotrophin antibodies on placental derived baboon trophoblast cells in vitro.

Immunization against chorionic gonadotrophin (CG) can terminate pregnancy in a number of species but the mechanisms responsible for this are poorly understood. Baboon CG has recently been purified and antibodies against this molecule were used in an in vitro system to study their effects on cultured trophoblast cells derived from placentae at 33 days of gestation. Secretion of bCG was measured by radioimmunoassay and the origin of this material was studied using immunohistochemical procedures. Heterologous antibodies against CG were introduced on day 5 of culture. Trophoblast cells appeared to secrete a CG material which was detectable in the daily spent medium and was localized within the trophoblast cells. Addition of antibodies caused cell lysis which was complement dependent. It was concluded that CG was localized on the baboon trophoblast cells and that antibodies against bCG caused complement dependent cell lysis.

Animals↗