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PubMed1985

The expression of major histocompatibility complex antigens by trophoblast in ectopic tubal pregnancy.

The reactivity of the various trophoblast populations found in ectopic fallopian tube pregnancy with established trophoblast-reactive markers and monoclonal antibodies to MHC antigens has been studied. In ectopic tubal pregnancy fetal trophoblast shows an identical reaction pattern with these antibodies to that seen in intrauterine pregnancy, suggesting that ectopic implantation is not related to an inherent immunological abnormality of fetal trophoblast. However, from this and other studies, it appears that extravillous trophoblast displays an unusual class I MHC antigenic structure. This observation may explain the ability of class I MHC--bearing fetal trophoblast--to survive both in the uterus and at an abnormal implantation site.

Antibodies, Monoclonal↗

PubMed1993

The effects of cytokines on human chorionic gonadotropin (hCG) production by a trophoblast cell line.

The present study was conducted to investigate the effects of cytokines on human chorionic gonadotropin (hCG) and its alpha- and beta-subunit release as well as protein synthesis in a trophoblast cell line. The human choriocarcinoma cell line, Jar, was used as a trophoblast model. Jar cells were incubated for 24 h with varying concentrations (5 x 10(-4)-40 micrograms/ml) of the following cytokines: Il-1, Il-2, Il-3, Il-4, Il-5, Il-6, IFN-gamma, tumor necrosis factor (TNF)-alpha, M-CSF and GM-CSF. Supernatants were assayed for hCG and its alpha- and beta-subunits by immunoradiometric methods. Cytotoxic effects were assessed by trypan blue staining. Protein synthesis was measured by [3H]leucine incorporation. The cytokines Il-1 and TNF-alpha significantly stimulated hCG release. The other cytokines had no significant effect on hCG production. Protein synthesis by the Jar cells was not significantly affected by either Il-1 or TNF-alpha. However, IFN-gamma (40 micrograms/ml) significantly suppressed protein synthesis by the Jar cells. Trophoblast viability in the presence of TNF-alpha (10 micrograms/ml) and IFN-gamma (40 micrograms/ml) was only 40% and 50%, respectively. These results suggest that cytokines may be important regulators of trophoblast function. Il-I appears to have a stimulatory effect on trophoblast hCG release, while TNF-alpha and IFN-gamma appear to have cytotoxic effects on trophoblast cells.

Biomarkers↗

PubMed1996

Human decidual leukocytes do not proliferate in response to either extravillous trophoblast or allogeneic peripheral blood lymphocytes.

The maternal leukocytes present in human decidua during the early weeks of pregnancy are composed of CD56+ NK cells (approximately 80%), CD3+ T cells (approximately 10%), and CD14+ macrophages (approximately 10%). These leukocytes are present in large numbers at the implantation site where trophoblast invades. The migrating extravillous trophoblast (EVT) cells express HLA class I antigens HLA-G and HLA-C. To examine whether EVT or other allogeneic cells are capable of inducing a local proliferative response in maternal decidual leukocytes, we have assayed [3H]thymidine incorporation by decidual leukocytes co-cultured with irradiated trophoblast or peripheral blood lymphocytes (PBL). No proliferative response was seen in decidual leukocytes either to trophoblast or to PBL as stimulators. In addition trophoblast did not stimulate a proliferative response in PBL. These findings indicate that extravillous trophoblast is not capable of initiating a classical immune response at the implantation site.

Cell Division↗

PubMed1994

Cytochrome P-450scc activity and substrate supply in human placental trophoblasts.

The degree of saturation of cytochrome P-450scc with cholesterol and the substrate turnover number of the cytochrome in cultured trophoblasts and mitochondria from the human placenta were investigated. Cholesterol sulfate was found to be a suitable substrate for probing the degree of saturation of cytochrome P-450scc with substrate during culture and in isolated mitochondria, since it enabled the maximum velocity of the cholesterol side-chain cleavage reaction to be estimated. In contrast, 25-hydroxycholesterol and low density lipoprotein supported trophoblast progesterone production at lower rates than that measured with saturating cholesterol sulfate. In the absence of exogenous substrate, the highest rate of progesterone synthesis by trophoblasts was observed at the beginning of the culture. With cholesterol sulfate as substrate, the turnover number of cytochrome P-450scc in cultured cells was 2.8 min-1 and was not significantly different to the turnover number of the cytochrome for placental mitochondria, where cholesterol is known to be saturating. Results indicate that cholesterol is limiting for progesterone synthesis in cultured trophoblasts even in the presence of lipoprotein rich medium and 8-bromo-cAMP. The concentration of cytochrome P-450scc in trophoblasts was only 20% of that measured for placental homogenate suggesting an induction of the cytochrome occurs when the trophoblasts fuse in vivo to form syncytiotrophoblasts.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1994

Cytochrome P-450scc activity and substrate supply in human placental trophoblasts.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2004

SAPKgamma/JNK1 and SAPKalpha/JNK2 mRNA transcripts are expressed in early gestation human placenta and mouse eggs, preimplantation embryos, and trophoblast stem cells.

OBJECTIVE: To test early-gestation human placenta, a human trophoblast cell line, mouse eggs, preimplantation embryos, and a mouse trophoblast cell line for the expression of mRNA transcripts for stress-activated protein kinase/c-Jun N-terminal kinase (SAPKgamma/JNK1, SAPKalpha/JNK2, and SAPKbeta/JNK3). DESIGN: Whole RNA was isolated from the tissue sources listed above and control tissues, and reverse transcription-polymerase chain reaction (RT-PCR) was performed to assay for the qualitative and semiquantitative presence of SAPKgamma/JNK1, SAPKalpha/JNK2, and SAPKbeta/JNK3. SETTING: None. PATIENT(S): None. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): The presence and magnitude of amplimer amounts in gels or gene hybridization on Affymetrix cDNA arrays of RT-PCR products of reactions for SAPKgamma/JNK1, SAPKalpha/JNK2, and SAPKbeta/JNK3. RESULT(S): SAPKgamma/JNK1 and SAPKalpha/JNK2 mRNA transcripts are present in early-gestation human placenta, a human trophoblast cell line, mouse eggs, preimplantation embryos, and a mouse trophoblast cell line at levels similar to positive control levels. SAPKalpha/JNK2 is expressed at the highest level of the three transcripts in the family. SAPKbeta/JNK3 is present at levels that are 1/100-1/1,000 those of the positive control and in some cases at the apparent level of the negative control (previously measured by the less-sensitive Northern blot analysis). Analysis with an Affymetrix cDNA array suggested that SAPKalpha/JNK2 and 38 kDa mitogen-activated protein kinase had the highest mRNA expression measured for each of three family members. CONCLUSION(S): Mitotic placental trophoblast cell lines and primary conceptus/embryo samples containing early placental trophoblasts express SAPKalpha/JNK2 at higher levels than SAPKgamma/JNK1, but not (only low background levels of) SAPKbeta/JNK3 mRNA transcripts. This suggests that SAPKgamma/JNK1 and SAPKalpha/JNK2 may be important mediators of stress-induced responses in early implanting conceptuses that could mediate embryo loss.

Animals↗

PubMed2005

Establishment and characterization of a human first-trimester extravillous trophoblast cell line (TEV-1).

OBJECTIVE: Research into the biology of human trophoblast invasion has been hampered by a lack of in vitro models. The aim of this study was to establish and characterize a human extravillous trophoblast cell line from the first-trimester placenta. METHODS: Human papillomavirus type 16 (HPV16) E6/E7 genes were stably expressed in primary cultures of first-trimester placenta via a retroviral vector (pLXSN-E6/E7). Several clones were characterized for extravillous trophoblastic properties by reverse transcriptase polymerase chain reaction (RT-PCR), Western blotting, and immunocytochemistry. The activities of matrix metalloproteinase (MMP)-2 and MMP-9 were examined with gelatin zymography. One clone (TEV-1), which retains all the established criteria for extravillous trophoblasts, was used in microarray analysis with Stanford Human cDNA chip (41, 421 cDNA features) to examine the differential gene expression after treatment of transforming growth factor beta 1 (TGFbeta1). The responsive gene to TGFbeta1 treatment was confirmed by quantitative real-time PCR. RESULTS: The clonal TEV-1 has been passaged for more than 105 population doublings with no sign of senescence, the activation of telomerase at early passages, and a near-diploid karyotype. TEV-1 cells expressed cytokeratin 7, HLA-G (a histocompatibility antigen, class IB), and CD9 (the cluster of differentiation antigen 9), and secreted active MMP-2 and MMP-9. TGFbeta1 treatment altered the gene expression profile of TEV-1 cells with a marked up-regulation of insulin-like growth factor binding protein 3 (IGFBP3), which was confirmed by quantitative real-time PCR. In addition, the TEV-1 was nontumorigenic when injected into nude mice and unable to form colonies in soft agar. CONCLUSION: Phenotypic and biologic characteristics of TEV-1 were shown as the properties of extravillous trophoblasts; thus, the TEV-1 cell line may be used as a cell model in extravillous trophoblast studies.

Cell Line↗

PubMed2006

Trophoblast fusion: fusogenic proteins, syncytins and ADAMs, and other prerequisites for syncytial fusion.

Trophoblast fusion in the placenta is an event of major importance for the preservation of a healthy pregnancy. This process takes place throughout pregnancy and is crucial for the maintenance of the syncytiotrophoblast layer, the direct border between maternal blood and fetal tissues. Different regulatory proteins have been reported that are involved in trophoblast fusion. Syncytin-1 is a candidate regulator of fusion together with its receptors ASCT2 (RDR) and ASCT1. Little is known about the receptor properties and the interactions between receptor and ligand. Syncytin-2 or HERV-FRD is another strong candidate also of retroviral origin; while its actual function still remains to be explored. ADAM12 has been proposed to be a candidate regulator of trophoblast fusion since it is known to be involved in myoblast fusion, a process with a variety of similarities to trophoblast fusion. Beside these regulatory proteins, there is the necessity of a flip of phosphatidylserine from the inner to the outer leaflet of the plasma membranes of the fusing cells. Moreover, appropriate events of the early and still reversible stages of the apoptosis cascade are indispensable for trophoblast fusion. In this review, we present some details on the above events and proteins with their most important properties that could explain their roles in trophoblast fusion.

ADAM Proteins↗

PubMed2005

Fibrin enhances differentiation, but not apoptosis, and limits hypoxic injury of cultured term human trophoblasts.

We hypothesized that fibrin enhances apoptosis and modulates differentiation of trophoblast in vitro. Cytotrophoblasts isolated from normal term human placentas were cultured < or =72 h in DMEM-10%-FBS on a fibrin matrix in standard or hypoxic conditions. Trophoblasts were cultured on plastic (control), type I collagen (matrix control), or dishes with fibrinogen, fibrin degradation products (FDP), thrombin, plasma fibronectin or cellular fibronectin. Apoptosis was determined by western analysis of the cleavage products of poly-ADP-ribose polymerase and cytokeratin 18 and caspase 3 activity. Cell cycle regulation was quantified by expression of proliferating cell nuclear antigen (PCNA) and p27 protein. Differentiation was determined by media level of hCG and hPL. Compared to the two controls, fibrin matrix had no effect on trophoblast apoptosis or total cell death in standard conditions. Neither fibrin nor collagen altered expression of PCNA or p27. In contrast, fibrin significantly increased the secretion of both hCG and hPL. Fibrin, but not FDP, thrombin or fibronectins, promoted hormonal differentiation. Fibrin limited the impact of a < or =8h of hypoxia on trophoblast hormone release but did not avert the effects of 24h of low oxygen and did not alter apoptosis in hypoxic trophoblast. We conclude that fibrin provides an environment conducive for trophoblast re-epithelialization of the surface of villi, where injury is marked by fibrin deposition.

Apoptosis↗

PubMedDate not supplied

The kinase p38 regulates peroxisome proliferator activated receptor-gamma in human trophoblasts.

Deficiency of either the mitogen-activated protein kinase p38 or the nuclear receptor PPARgamma results in disrupted vasculogenesis and abnormal development of the murine placenta. In addition, PPARgamma regulates differentiation of human trophoblasts. Here we tested the hypothesis that p38 plays an important role in the regulation of PPARgamma in primary human trophoblasts. We initially confirmed that cultured trophoblasts derived from normal term human placentas express p38 as well as its functional phosphorylated form. Whereas PPARgamma did not alter p38 expression, p38 inhibitors diminished the transcriptional activity of PPARgamma in primary trophoblasts. In addition, inhibition of p38 resulted in marked attenuation of PPARgamma-stimulated hCG production by cultured trophoblast. Our data support an effect of p38 on PPARgamma protein stability because p38 inhibition led to reduced expression of PPARgamma protein without a significant effect on PPARgamma mRNA, and this reduction was blocked by the protease inhibitor MG-132. Together, these data indicate that p38 regulates PPARgamma expression and activity in term human trophoblasts. Cross talk between p38 and PPARgamma signaling may play a role in modulating differentiation and function of the human placenta.

Cells, Cultured↗

PubMed2003

Infection, replication, and cytopathology of human papillomavirus type 31 in trophoblasts.

Human papillomavirus (HPV) DNA is preferentially found in spontaneous abortions, specifically residing in trophoblasts, and transfected HPV-16 DNA replicates and produces progeny in 3A trophoblasts in culture. In this study 3A trophoblasts were shown to display both HPV receptors and infection by HPV-31b and HPV-6 virus resulted in de novo (increasing) HPV DNA replication in these cells (inhibited by neutralizing anti-HPV31b antibodies). Reverse transcription-polymerase chain reaction analysis revealed that E1;E4, E6, and L1 were significantly expressed at days 5 (early) and 10 (late), respectively, and in situ immunocytochemistry verified L1 protein expression. Perhaps most important, HPV 31b virus infection caused both a decrease in 3A trophoblast cell numbers in a dose-dependent manner and a low trophoblast-endometrial cell adhesion (both inhibited by neutralizing anti-HPV-31 antibodies). These data further support the hypothesis that HPVs are fully active in trophoblasts and may cause some spontaneous abortions.

Cell Adhesion↗

PubMed2004

Connexin31-deficient trophoblast stem cells: a model to analyze the role of gap junction communication in mouse placental development.

The connexin (Cx) expression during placental development in rodents is subject to exacting spatiotemporal regulation. Following implantation, Cx31 characterizes the early trophoblast cell lineage and is expressed by the spongiotrophoblast during placental development until birth. Inactivation of the Cx31 gene results in a transient placental dysmorphogenesis with an imbalance in the trophoblast cell lineage differentiation in favor to giant cells [Dev. Biol. 231 (2001) 334]. In this study, we show that trophoblast stem (TS) cells exhibit the same connexin expression found in trophoblast cell lineage differentiation. Undifferentiated TS cells exclusively express Cx31 protein and Cx31.1 transcripts. Upon differentiation of TS cells, placental-specific Cx26 and Cx43 are induced. Cx31 knockout TS cells revealed an accelerated differentiation process to giant cells compared to controls, indicated by an overall shift in expression of connexins and marker genes such as Mash2, Pl-1, and Tpbpa. Moreover, proliferation was significantly reduced in Cx31 knockout TS cells upon differentiation. Both wild type and Cx31 knockout TS cells are able to invade and erode host vessels when injected into nude mice. We conclude that during trophoblast cell lineage differentiation, the Cx31 gap junction channel is involved in maintaining the proliferative diploid trophoblast cell population.

Animals↗

PubMed2004

Trophoblast interactions with endothelial cells are increased by interleukin-1beta and tumour necrosis factor alpha and involve vascular cell adhesion molecule-1 and alpha4beta1.

Interactions between fetal extravillous trophoblast cells and maternal uterine cells are of critical importance in successful placentation. In the first trimester, trophoblasts invade the uterine environment and reach the spiral arteries where they interact with vascular cells; however, little is known of the nature of these interactions. We have developed a fluorescent binding assay to investigate the contact between trophoblasts and endothelial cells and to determine its regulation by cytokines and adhesion molecules. Stimulation of an endothelial cell line (SGHEC-7) with interleukin-1beta or tumour necrosis factor-alpha significantly increased adhesion of the first-trimester extravillous trophoblast-derived cell line, SGHPL-4. Using blocking antibodies, vascular cell adhesion molecule-1 (VCAM-1) and integrin alpha4beta1 (VLA-4), but not intercellular adhesion molecule-1 (ICAM-1), were shown to be important in trophoblast binding to activated endothelial cells. SGHPL-4 cells were shown to express HLA-G, alpha4beta1 and ICAM-1 at high levels and LFA-1 and VCAM-1 at lower levels. ICAM-1 and VCAM-1 are expressed on SGHEC-7 cells and their expression was confirmed on primary decidual endothelial cells. In conclusion, we have demonstrated the importance of VCAM-1 and alpha4beta1 in trophoblasts-endothelial interactions. Improved knowledge of the nature of these fetal-maternal interactions will have implications for understanding situations when placentation is compromised.

Cell Line↗

PubMed1984

In vitro production of pregnancy-associated plasma protein A by human decidua and trophoblast.

Immunohistochemical techniques and direct measurements of pregnancy-associated plasma protein A (PAPP-A) have demonstrated the presence of PAPP-A in trophoblast and decidua. The purpose of the present study was to investigate the possibility that these tissues are capable of producing PAPP-A in vitro. Trophoblast and decidua were obtained from term deliveries and from legal surgical terminations of pregnancy (7 to 12 weeks). In addition to trophoblast and decidua, myometrium was also obtained during two hysterectomies in the first trimester of pregnancy. Tissues were incubated in medium 199 at 37 degrees C under an oxygen/carbon dioxide atmosphere. Media containing either pregnancy-associated serum or non-pregnancy-associated serum were changed after 8 hours of incubation in medium 199 alone. In addition to PAPP-A, human placental lactogen (hPL) and prolactin (Prl) were measured in homogenates and media by radioimmunoassays in order to confirm the viability of the cultured tissues. Addition of pregnancy-associated serum to the media induced a significant release of PAPP-A from trophoblast and decidua when compared to that in control cultures. Non-pregnancy-associated serum had no effect. Myometrium did not release any measurable PAPP-A into the medium even in the presence of pregnancy-associated serum. Cycloheximide added to pregnancy-associated serum significantly inhibited the release of PAPP-A from trophoblast and decidua. These last tissues, irrespective of the culture condition, released significantly more PAPP-A as well as hPL and Prl than was initially present in the tissue. These data demonstrate that PAPP-A is released in vitro by trophoblast and decidua (but not by myometrium) and that this release can be magnified by a factor present only in pregnancy-associated serum. The release of PAPP-A, hPL, and Prl is considered as a de novo production since concentration of these proteins are higher in media and tissues after incubation compared to concentrations initially present in the tissue before culture and since cycloheximide significantly inhibits the release of PAPP-A, Prl, and hPL from the cultured tissues.

Culture Media↗

PubMed1996

Treatment of low-risk metastatic gestational trophoblastic tumors with single-agent chemotherapy.

OBJECTIVE: Our purpose was to evaluate the efficacy and toxicity of single-agent chemotherapy and to identify risk factors associated with chemotherapy resistance in the treatment of low-risk metastatic gestational trophoblastic tumors. STUDY DESIGN: We reviewed the records of all patients with gestational trophoblastic tumors treated with single-agent chemotherapy at the John I. Brewer Trophoblastic Disease Center of Northwestern University between 1962 and 1992. A total of 92 patients with low-risk metastatic gestational trophoblastic tumors by National Cancer Institute criteria were identified. Patients received methotrexate (n = 61), actinomycin D (n = 4), alternating methotrexate and actinomycin D (n = 5), or hysterectomy with methotrexate (n = 20) or actinomycin D (n = 2). RESULTS: All 92 patients with low-risk metastatic gestational trophoblastic tumors were cured. Primary remission was achieved with initial single-agent therapy in 62 patients (67.4%). A second sequential single agent was used because of drug resistance in 20 patients (21.7%) or drug toxicity in 10 patients (10.9%). Only one patient (1%) needed multiagent chemotherapy to be cured. Adjuvant hysterectomy was performed in 22 patients (23.9%). Surgery was not required to remove resistant tumor foci. Chemotherapy toxicity, most commonly stomatitis, occurred in 36 patients (39.1%), but none of these effects was life threatening. Large vaginal metastasis was the only identifiable factor significantly associated with failure of initial single-agent chemotherapy (p = 0.03). CONCLUSION: In this large series of patients with low-risk metastatic gestational trophoblastic tumors, sequential single-agent chemotherapy with methotrexate and actinomycin D provided safe and extremely effective treatment.

Adolescent↗

PubMed1996

Uptake of human immunodeficiency virus envelope protein gp120 by human trophoblast in culture.

OBJECTIVE: Our purpose was to determine whether human trophoblast has a cell surface CD4 antigen that will bind to gp120, the envelope protein of human immunodeficiency virus. STUDY DESIGN: Uptake of iodine 125-labeled gp120 by trophoblast in culture was measured. Particular attention was paid to technical details that may have caused the contradictory results reported by previous investigators: the source of the recombinant gp120, the method of radioiodination, and the isolation procedure of trophoblast to ensure elimination of contaminating cells, particularly macrophages. RESULTS: Uptake of transferrin-free iodine 125-labeled gp120 to trophoblast was unaffected by adding a 200 molar excess of gp120, by preincubating gp120 with soluble CD4 to block the CD4 binding sites on gp120 and by preincubation of trophoblast with a blocking antibody to CD4 (OKT4a). In contrast, uptake of gp120 by CD4-positive H9 human lymphocytes was reduced 79% by a 200 molar excess of gp120 and > 50% by a CD4-blocking antibody. CONCLUSIONS: Uptake of gp120 to trophoblast is by a high capacity, CD4-independent mechanism that is probably nonspecific and may be related to the mechanism for binding other circulating glycoproteins in maternal blood.

Animals↗

PubMed1998

Absence of expression of RhD by human trophoblast cells.

OBJECTIVE: Our purpose was to determine whether the RhD gene is expressed in trophoblast at any stage of gestation. STUDY DESIGN: Trophoblast and fetal tissue were obtained from 18 pregnancies at 8 to 40 weeks' gestation. Deoxyribonucleic acid and ribonucleic acid were extracted from trophoblast. Complementary deoxyribonucleic acid was synthesized from ribonucleic acid, and reverse transcriptase-polymerase chain reaction was performed using primers specific for the RhD gene. Deoxyribonucleic acid was extracted from fetal tissue to determine the fetal RhD status by means of polymerase chain reaction. Antigen expression was also sought by analytic cytometric analysis (flow cytometry and immunocytochemistry) using a monoclonal anti-D antibody. RESULTS: Trophoblast was studied from various combinations of RhD-positive and RhD-negative fetuses (on deoxyribonucleic acid) from mothers to find no RhD gene expression in any sample. Flow cytometry and immunocytochemistry confirmed this by demonstrating no RhD antigen sites on trophoblast cells. CONCLUSION: Contrary to a previous report, we conclude that the RhD gene is not expressed in human trophoblast in any trimester.

DNA↗

PubMed1999

Hypoxia limits differentiation and up-regulates expression and activity of prostaglandin H synthase 2 in cultured trophoblast from term human placenta.

OBJECTIVE: We determined the effect of hypoxic conditions on cellular differentiation and prostaglandin H synthase expression in cultured human term trophoblast. STUDY DESIGN: Cytotrophoblasts isolated from term placentas were cultured for 24-72 hours in a standard (20% oxygen) or hypoxic (1% to 2% oxygen) atmosphere. Trophoblast biochemical differentiation was determined by release of human chorionic gonadotropin. Morphologic differentiation was evaluated by epifluorescent and confocal microscopic examination of cultures after dual cytochemical staining for surface membrane desmosomes and intracytoplasmic nuclei. Prostaglandin H synthase 2 expression was determined by Western blot analysis and correlated with enzyme activity by immunoassay of 2 prostaglandin H synthase 2 products, prostaglandin E2 and thromboxane. RESULTS: Human chorionic gonadotropin levels in media and syncytiotrophoblast formation were markedly diminished in trophoblast cultured in hypoxia, compared with trophoblast in control cultures, whereas viability was unchanged. Hypoxia up-regulated expression of trophoblast prostaglandin H synthase 2 but not of prostaglandin H synthase 1 and increased prostaglandin E2 and thromboxane release. CONCLUSIONS: Hypoxia limits differentiation and enhances prostaglandin H synthase 2 expression in cultured villous trophoblast. These responses may account for the cytotrophoblast prominence characteristic of placentas exposed to attenuated oxygen delivery.

Blotting, Western↗