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PubMed1999

Paracrine regulation of distinct trophoblast functions in vitro by placental macrophages.

In view of the accumulating evidence for paracrine mechanisms regulating trophoblast function, we tested the hypothesis that placental macrophages affect trophoblast activity in a paracrine fashion. Trophoblast was isolated from 17 term placentas (-IP). One aliquot of cells was further immunopurified (+IP) using an HLA class I antibody. This increased the proportion of trophoblast (+IP >97%; -IP approximately 70%) as identified by rigorous immunocytochemistry. Most (approximately 70%) non-trophoblast cells in -IP were macrophages. The cells were cultured for 5 days with a daily medium change. In addition, +IP cells from seven placentas were cultured with lipopolysaccharide (LPS)-stimulated or -unstimulated macrophage-conditioned media. The concentrations of lactate, trophoblast-specific hormones, human chorionic gonadotropin-beta (hCG-beta) and human placental lactogen (hPL), of several prostanoids and of endothelin-1 and angiotensin II were determined in the culture media. The accumulated amounts of substances released into the culture media, corrected for the greater proportion of trophoblast in +IP cultures, were on average two- to threefold higher (hCG-beta: 18-fold) in +IP than in -IP, with the exception of endothelin-1,2 (no change), angiotensin II (-70%) and 6-keto-prostaglandin-F1alpha (-40%). [3H]leucine incorporation into the trichloroacetic acid (TCA)-precipitable pool measured on day 5 was twofold higher in +IP than in -IP. Addition of conditioned media reverted these changes. The data demonstrate that placental macrophages in culture affect trophoblast biosynthetic activity in a paracrine fashion. We conclude that macrophages are important regulators of trophoblast activity.

Cell Communication↗
PubMedDate not supplied

From 13 weeks to term, the trophoblast of human placenta grows by the continuous recruitment of new proliferative units: a study of nuclear number using the disector.

A method is presented for obtaining assumption-free estimates of the number of nuclei in the trophoblast of the human placenta and for defining the size of the trophoblast proliferative unit (TPU). The method relies on the disector, a stereological device for counting arbitrary particles in 3-dimensional space using pairs of parallel sections separated by a known distance. It is applied to investigate factors which contribute to trophoblast growth from 13 weeks of gestation to term. Physical disectors were sampled systematically using adjacent 4-4.6 microns thick paraffin sections. Nuclei in the trophoblast (syncytial and cellular) were counted if they appeared in an unbiased counting frame on one section but were absent from the adjacent section. Nuclear packing densities were converted to absolute numbers of nuclei by using placental volume as the reference space. At 37-39 weeks, the average placenta contained 6.4 x 10(10) trophoblast nuclei of which 90 per cent were located within the syncytium and the remainder in the cytotrophoblast. From a knowledge of total trophoblast volume, it was found that each nucleus is associated with 970 microns3 of trophoblast and each cytotrophoblast cell with 11,000 microns3. The latter may be regarded as the volume of a TPU. From 13 weeks of gestation to term, there was a ninefold increase in nuclear number but the trophoblast volumes associated with nuclei, including the size of the TPU, remained constant. Growth of trophoblast is purely hyperplastic and occurs by recruitment of new TPUs.

Cell Division↗
PubMed2005

Extravillous trophoblast apoptosis--a workshop report.

During normal pregnancy, extravillous trophoblast cells invade maternal uterine tissues. The interstitial trophoblast penetrates decidual tissues reaching the inner third of the myometrium. A subset of the interstitial trophoblast, the intramural/endovascular trophoblast transforms uterine spiral arteries into large-bore conduits to enable the adequate supply of nutrients and oxygen to the placenta and thus the fetus. Control of invasion is still a mystery and therefore, in this workshop report already existing concepts as well as new models are discussed. Maternal cells such as macrophages and endothelial cells have a clear impact on trophoblast invasion and apoptosis. However, the trophoblast cells need to be susceptible to undergo apoptosis. Thus, an intrinsic program within the trophoblast needs to be activated before induction from the outside can be successful. Quantification of apoptosis further clarified that apoptosis of interstitial trophoblast is not the ultimate means to lead to pathologically shallow invasion. On the other hand, apoptosis of intramural/endovascular trophoblast seems to be highly relevant for a correct transformation of spiral arteries.

Animals↗
PubMed2005

Aberrations of early trophoblast differentiation predispose to pregnancy failure: lessons from the anti-phospholipid syndrome.

OBJECTIVES: The epithelium of the human placenta comprises an inner cytotrophoblast (CT) which proliferates and fuses with the outer differentiated syncytiotrophoblast (ST). Turnover has been studied focussing on second and third trimester placentas but with a paucity of data describing the normal first trimester trophoblast. The aim of this study was to compare the nuclear CT:ST ratio in normal and pathological pregnancy and thus establish the relationship between cytotrophoblast and syncytiotrophoblast nuclear number during early gestation. METHODS: Archival first trimester material from placentas from healthy pregnancy and recurrent miscarriage (anti-phospholipid syndrome) was stained with H&E, cytokeratin-7 and Mib-1. The area of trophoblast as a fraction of total villous area was calculated and the number of sectioned cytotrophoblast and syncytiotrophoblast nuclei as well as the number of proliferating cytotrophoblast was evaluated. RESULTS: Normal features of trophoblast development during the first trimester (rise in trophoblast area, increase in number of syncytiotrophoblast nuclei, increase in number of proliferating cytotrophoblast, decrease in the nuclear CT:ST ratio) are absent/reversed in tissues from recurrent miscarriage (decreasing trophoblast area, constant number of syncytiotrophoblast nuclei, decreasing number of proliferating trophoblast, constant nuclear CT:ST ratio). CONCLUSIONS: Proliferation of cytotrophoblast in early gestation provides a pool of trophoblast stem cells critical for ongoing placental development. Premature cytotrophoblast differentiation in favour of syncytial fusion results in deficiencies of cytotrophoblast and rarification of villous trophoblast. Abnormal trophoblast differentiation in early gestation may be due to a premature onset of maternal perfusion of the placenta and may be a likely antecedent for conditions associated with failure of placentation such as recurrent miscarriage.

Abortion, Habitual↗
PubMed1994

Cell-mediated immunity to trophoblast antigens in women with recurrent spontaneous abortion.

OBJECTIVES: The purpose of this study was to determine whether trophoblast antigens activate cell-mediated immune responses in women with recurrent abortion of unknown cause by inducing lymphocyte proliferation and to correlate this with embryotoxic factor production. STUDY DESIGN: Mononuclear cells were isolated from 57 nonpregnant women with recurrent abortion of unknown cause and from 10 fertile controls with normal reproductive histories. Lymphocyte proliferation assays were performed with trophoblast antigen extracts from the human choriocarcinoma cell lines Jeg-3 and JAR, fractionated trophoblast antigens, and for control, red blood cell membrane antigens. A stimulation index > 3 was considered significant stimulation. Trophoblast-stimulated culture supernatants were also tested for embryotoxic activity. RESULTS: Thirty (52.6%) women with recurrent abortion of unknown cause responded to trophoblast antigen stimulation with a stimulation index > 3, whereas none of the control group responded. Neither patients with recurrent abortion nor women with normal reproductive histories responded to red blood cell membrane antigen. The mean stimulation index in the trophoblast antigen lymphocyte proliferation assay was significantly higher in women with recurrent abortion than in women with normal reproductive histories (3.99 +/- 2.82 vs 1.64 +/- 0.34, p < 0.01). Antigen extracts from the cytosol and membrane fractions of Jeg-3 provided the strongest stimulation. Lymphocyte proliferation correlated with embryotoxic factor production; 90.0% of women with a stimulation index > 3 and none of the controls produced embryotoxic factors after stimulation with trophoblast antigens. CONCLUSION: In this study 52.6% of women with recurrent abortion of unknown cause compared with none in controls exhibited in vitro evidence of T-cell immunity to trophoblast antigen stimulation. Further work is needed to determine whether T-cell immunity to trophoblast is involved in the pathogenesis of recurrent spontaneous abortion.

Abortion, Habitual↗
PubMed2000

Angiopoietin-1 and angiopoietin-2 activate trophoblast Tie-2 to promote growth and migration during placental development.

Human placental development involves coordinated angiogenesis and trophoblast outgrowth that are compromised in intrauterine growth restriction (IUGR). As Tie-2((-/-)) mice exhibit growth retardation and vascular network malformation, the expression of Tie-2 and its ligands, angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2), were investigated in human placenta from normal pregnancies and those complicated by severe IUGR. Ribonucleotide protection assays showed no significant change in the expression of Ang-2 mRNA between gestationally matched normal and IUGR placentas; however, immunoblots revealed that Ang-2 protein was significantly decreased in IUGR, suggesting that this may contribute to the abnormal development of the villous vasculature. In situ hybridization studies showed that Ang-1 and Tie-2 were detected in the cyto/syncytiotrophoblast bilayer in first-trimester placenta, whereas Ang-2 mRNA was restricted to the cytotrophoblast, suggesting their role in trophoblast function. At term, Ang-1 mRNA and immunoreactive protein were restricted to the paravascular tissues of the primary stem villi, supporting its role in vessel maturation. In contrast, Ang-2 was expressed throughout the term villous core, perhaps to permit the developing placental vascular network to remain in a state of fluidity. As these studies also revealed that trophoblast, in addition to endothelial cells, expressed Tie-2 receptors, we investigated the potential role of Ang-1/Ang-2 on trophoblast proliferation, migration, and the release of NO. Using spontaneously transformed first-trimester trophoblast cell lines that exhibit cytotrophoblast-like (ED(27)) and extravillous trophoblast-like (ED(77)) properties, we show that the addition of Ang-2 (250 ng/ml) stimulated DNA synthesis in ED(27) trophoblast cells and triggered the release of NO. Ang-1 stimulated trophoblast (ED(77)) migration in a dose-dependent manner that was inhibited by recombinant Tie-2-FC. These data thus imply, for the first time, a specific role for angiopoietins as regulators of trophoblast behavior in the development of the utero/fetoplacental circulation, an action independent of their well-established roles in vascular endothelium.

Angiopoietin-1↗
PubMedDate not supplied

Differential interferon production in human first and third trimester trophoblast cultures stimulated with viruses.

Stimulation of human placental first and third trimester trophoblast and syncytiotrophoblast cultures with viruses [Newcastle Disease Virus (NDV) and Sendai virus] led to a high interferon (IFN) production. The magnitude of the production was dependent on the gestational age of the trophoblast, type of inducer and the stage of differentiation of the trophoblast. The data obtained indicated that the first trimester trophoblast cultures produced five to sixfold more IFN than the third trimester trophoblast on per cell basis whereas syncytiotrophoblast at term produced twice as much IFN than the mononuclear term trophoblast when stimulated with the viruses. NDV and Sendai virus produced different levels and composition of IFN-alpha and -beta in both first and third trimester trophoblast and syncytiotrophoblast cultures. Purification of the virus-induced trophoblast interferons (tro-IFNs) by tandem high-performance affinity chromatography resulted in specific activities between 0.7 and 2.7 x 10(8) IU/mg of protein when assayed on human amniotic WISH cells. The tro-IFN-alpha protected both human and bovine MDBK cells from virus infection whereas the tro-IFN-beta protected only the human cell lines tested. The possible roles of the tro-IFNs are discussed in light of the observed differences in trophoblast IFN response.

Cells, Cultured↗
PubMedDate not supplied

Detection of human and murine trophoblast-specific antigens and an assessment of their species specificity.

The distribution and species specificity of human and mouse trophoblast-specific surface antigens detected by heterologous anti-mouse ectoplacental cone (anti-EPC) trophoblast and anti-human first-trimester trophoblast plasma membrane (anti-TrPM) antisera were assessed using several immunochemical and immunolabelling assays. The findings with immunofluorescence assays using anti-EPC antiserum on monolayer cultures indicate that the expression of mouse trophoblast-specific antigens is restricted to the major trophoblast components of the mouse placenta, as well as pre- and early post-implantation trophoblast, and does not occur on fetal, amnion or tumour tissues. The anti-EPC antiserum does not cross-react with human chorionic villous trophoblast. The human trophoblast-specific antigens also displayed species specificity. The anti-TrPM antiserum showed no evidence of cross-reactivity with rhesus monkey, rabbit, guinea pig or mouse trophoblast by immunodiffusion, crossed immunoelectrophoresis, immunofluorescence or immunoperoxidase labelling.

Animals↗
PubMed1996

Quantitative analysis of the spreading of the mouse trophoblast in vitro: a model for early invasion.

The outgrowth of the mouse blastocyst in culture represents an in vitro model of trophoblastic invasion. In the present study we analysed trophoblast spreading by time lapse video microscopy. Trophoblast spreading consists of (1) the migration and (2) the giant cell transformation of trophoblast cells, (3) the proliferation of ectoplacental cone (EPC) cells and (4) the subsequent transformation of EPC cells into the secondary giant cells. During migration, ruffling of the trophoblast cell membrane is followed by the formation of lamellipodia. The mean surface areas of the spreading trophoblast, measured in more than 100 cultured blastocysts, increased linearly from 48 to 96 h of culture, while the linear migratory speed at the periphery of the outgrowth declined as the time of culture advanced. The EPC cells increased in size approximately eightfold during the giant cell transformation. The apparent nuclear:cytoplasmic ratios, i.e., ratios between the size of nucleus and that of the cytoplasm, measured as the surface areas on the photomicrographs, of EPC cells increased between 40-46 h of culture, but a sharp decline in the ratio occurred between 50 and 51 h of culture, reflecting either the sudden and tremendous increase in the cellular volume and/or spreading of the cytoplasm. The rates of trophoblast spreading varied considerably among the blastocysts of different genetic constitution examined (ICR, C57BL/6, C3H/He and (B6 x C3)F1. It was fastest in blastocysts obtained from matings of males and females of (B6 x C3)F1, and slowest in the C57BL/6 embryos. The differences in the rate of outgrowth observed may not simply be ascribed to difference in the developmental speed of the early embryos, because the rate of outgrowth reached a plateau at about 96-120 h and no "catch-up' was observed by leaving the blastocysts in culture longer. Our results strongly suggest the possible presence of genetic regulatory mechanisms underlying trophoblast outgrowth; further analysis of the phenomenon may provide clues to understand the molecular mechanisms of trophoblastic invasion during the early phase of implantation, hopefully leading to improved success rates of in vitro fertilization-embryo transfer.

Animals↗
PubMedDate not supplied

Changes in the distribution pattern of galectin-1 and galectin-3 in human placenta correlates with the differentiation pathways of trophoblasts.

Human placentation is a complex biological phenomenon that results from precisely regulated interactions between cells and the extracellular matrix. Galectin- 1 and galectin-3 belong to a newly defined family of galactose-binding lectins that can bind several glycoconjugates such as the basement membrane glycoprotein laminin, and are involved in many biological events including cell adhesion. In this study, the expression of these two galectins in first and third trimester normal human placenta was examined using single and double immunohistochemical staining and specific antibodies for galectins and cytokeratins. Galectin-3 was detected in all trophoblastic lineages including villous cytotrophoblasts and extravillous trophoblasts (trophoblastic cell columns, infiltrating trophoblasts, endovascular trophoblasts and placental bed giant cells). On the contrary, galectin-1 distribution was restricted to endometrium. A reduction of galectin-3 expression was observed from the villous trophoblasts to the trophoblastic cell columns. This pattern correlated with the switch from a proliferative to a migratory phenotype. Galectin-1 and galectin-3 were both detected in maternal decidual cells. Our data demonstrate a specific pattern of galectin-1 and galectin-3 expression in trophoblastic tissue, and suggest these lectins could contribute to cell-cell and cell matrix interactions of trophoblast during placentation.

Antigens, Differentiation↗
PubMed1997

Mechanisms of trophoblast-virus interaction.

The human placenta serves as a barrier to the transmission of some viruses, but allows others to reach the fetal circulation. The resistance and permissiveness of the placenta to viral transmission appears to be determined in large part by the placental trophoblast. In order to define the mechanisms by which human trophoblast cells influence vertical transmission of viruses, we have studied the interaction of replication-deficient recombinant viral vectors with transformed human choriocarcinoma (BeWo) cells and primary trophoblast cell cultures. Recombinant adenovirus vectors efficiently transduce BeWo cells and primary trophoblast cells. However, as BeWo cells differentiate after treatment with cAMP analogs, they become relatively resistant to adenovirus-mediated transduction due to diminished uptake of the virus particles. This differentiation-dependent loss of adenovirus transduction may be related to the down-regulation of the coxsackie adenovirus receptor, which we have detected in undifferentiated trophoblast cells. Recombinant herpes simplex virus vectors also transduce undifferentiated BeWo cells and isolated cytotrophoblast cells, but transduction by herpes simplex virus vectors declines with cAMP-induced trophoblast differentiation, apparently due to reduced viral uptake. In contrast, cAMP treatment augments trophoblast transduction by recombinant adeno-associated virus, a member of the parvovirus family. This augmentation appears to be due to increased virus uptake by a yet to be determined mechanism. The understanding of the molecular basis of these interactions between recombinant viral vectors and trophoblast cells may yield strategies to prevent vertical transmission of viruses as well as to create opportunities to modify trophoblast function through gene transfer using viral vectors.

Adenoviridae↗
PubMed1999

Trophoblast deportation in human pregnancy--its relevance for pre-eclampsia.

The maternal syndrome of pre-eclampsia is thought to result from endothelial cell damage caused by a circulating factor derived from the placenta. This study investigates the hypothesis that trophoblast deportation may be part of the process by which this factor enters the maternal circulation. The nature and incidence of trophoblast deportation was studied in uterine vein and peripheral blood taken from normal and pre-eclamptic women at caesarean section. Trophoblasts were enriched using immunomagnetic beads to deplete leucocytes and labelled with trophoblast-specific monoclonal antibodies. Syncytiotrophoblast, cytotrophoblast, cytotrophoblast clumps and anucleate trophoblast cells were found in uterine vein blood. Cytotrophoblast cells were found to be shed less frequently than syncytiotrophoblast and the majority were probably villous in origin. Trophoblasts were found in the uterine vein blood of normal pregnant women with higher levels in pre-eclampsia. However, trophoblasts were rarely found in the peripheral circulation. There was no correlation between trophoblast numbers and either the severity of the disease, the extent of placental pathology or the inhibitory effect of uterine and peripheral vein plasma on endothelial growth in vitro. Thus, it is speculated that increased trophoblast deportation in pre-eclampsia is secondary to the structural and functional changes occurring in the placenta, rather than directly linked with the circulating endothelial cell damaging factor in pre-eclampsia.

Adult↗
PubMedDate not supplied

Lateral placental growth occurs by trophoblast cell invasion of decidual veins.

During human pregnancy, growth of the placenta is proportionally greater than the growth of the decidual surface, suggesting that trophoblast cells invade the decidua at the placenta's margin. We hypothesized that a method of lateral placental growth was trophoblast cell invasion of decidual veins. This was investigated in two in situ pregnancies and in tissues from 100 women undergoing elective termination at 8-12 weeks of gestation. Decidua was compared to normal secretory endometrium. Histological sections were stained by immunohistochemistry to identify trophoblast cell and vascular antigens, as well as vascular cell adhesion molecule (VCAM), integrin subunits beta(1)and beta(4), and oncofetal fibronectin. Dilated veins were observed in all decidua but not in the secretory endometrium. Decidual and myometrial veins contained villi, trophoblast cell islands and syncytial elements. Decidual endothelial cells expressed vascular cell adhesion molecule (VCAM). Villous trophoblast cells were integrin subunits beta(4)positive and beta(1)negative. Trophoblast cell islands in the placenta and within decidual veins were integrin subunits beta(1)positive and beta(4)negative. Trophoblast cell islands and villi attached to veins, and mononuclear cells, invaded decidual stroma. Oncofetal fibronectin was present at sites of trophoblast invasion. These findings suggest that a method of lateral placental growth is trophoblast cell invasion of veins.

Cell Movement↗
PubMed2002

Adriana and Luisa Castellucci Award lecture 2001. Hypoxia inducible factor-1: oxygen regulation of trophoblast differentiation in normal and pre-eclamptic pregnancies--a review.

During early pregnancy, trophoblast differentiation occurs in an environment of relative low oxygen tension which is essential for normal embryonic and placental development. At around 10-12 weeks' gestation, when the intervillous space opens to maternal blood, there is an increase in Po(2). This increase correlates with the time of maximal trophoblast invasion into the maternal decidua, which allows extravillous trophoblast cells to access and remodel the maternal spiral arteries. Hypoxia Inducible Factor 1(HIF-1) is a transcription factor which activates gene transcription in response to varying oxygen concentration of cells. HIF-1 is a heterodimer composed of the inducible HIF-1alpha and the constitutively expressed HIF-1beta/ARNT subunits. Using villous explants, we have demonstrated that the oxygen-regulated events of early trophoblast differentiation are in part mediated by TGFbeta(3), an inhibitor of trophoblast differentiation, via HIF-1alpha. Pre-eclampsia is a disease of pregnancy that is characterized by shallow trophoblast invasion. Recently, we have reported that TGFbeta(3) is over-expressed in pre-eclamptic pregnancy and that its down-regulation restores invasive capability to trophoblast cells. Because TGFbeta(3) is downstream of HIF-1alpha, in the present study we investigated the expression of HIF-1alpha in pre-eclamptic placentae and age-matched controls using in situ hybridization and histochemical analyses. We found that HIF-1alpha mRNA and protein expression are abnormally elevated in pre-eclamptic placental tissue when compared to normal placental tissue. We conclude that pre-eclampsia may result from a developmental failure of oxygen to increase or of trophoblast cells to respond and/or sense an increase in oxygen. This will prevent the normal TGFbeta3 down-regulation and will lead to poor trophoblast invasion predisposing the pregnancy to pre-eclampsia.

Adult↗
PubMed2005

N-myc down-regulated gene 1 modulates the response of term human trophoblasts to hypoxic injury.

The placenta is susceptible to diverse insults during human pregnancy. The expression of the protein N-myc down-regulated gene 1 (NDRG1) is regulated during cell proliferation, differentiation, and in response to stress. Nevertheless, the function of this protein in humans remains unknown. We tested the hypothesis that NDRG1 is up-regulated in hypoxic primary human trophoblasts and that NDRG1 modulates trophoblast response to hypoxia. We initially demonstrated that the expression of NDRG1 is enhanced in primary human trophoblasts exposed to hypoxia. Importantly, we found a similar increase in NDRG1 expression in placental samples derived from either singleton gestations complicated by intrauterine growth restriction or from dizygotic twin gestation where one twin exhibited growth restriction. Having established efficient lentivirus-mediated transfection of primary human trophoblasts, we overexpressed NDRG1 in trophoblasts, which resulted in enhanced trophoblast differentiation. In contrast, lentivirus-driven short interfering RNA-mediated silencing of NDRG1 diminished trophoblast viability and differentiation. Consistent with these results, NDRG1 reduced the expression level of p53 in trophoblasts cultured in standard or hypoxic conditions. Furthermore, NDRG1 expression was regulated by the activity of SIRT1 (Sir2-like protein 1), which promotes cell survival. Together, our data indicate that NDRG1 interacts with SIRT1/p53 signaling to attenuate hypoxic injury in human trophoblasts.

Cell Cycle Proteins↗
PubMed1996

Prevalence and significance of implantation site trophoblastic atypia in hydatidiform moles and spontaneous abortions.

The authors studied the prevalence and significance of implantation site trophoblastic atypia in hydatidiform moles and spontaneous abortions. Three pathologists independently categorized 99 early abortion specimens regarding diagnosis (spontaneous abortion, partial hydatidiform mole, complete hydatidiform mole); qualitative atypia of implantation site trophoblast (absent, mild, moderate-severe); and quantitative atypia of implantation site trophoblast (absent, focal, diffuse). Interobserver agreement was good to excellent regarding diagnosis (kappa 0.66-0.79) and poor to fair regarding qualitative atypia of implantation site trophoblast (kappa 0.20-0.43). By consensus diagnosis, implantation site trophoblastic atypia was mild and focal in 5% of 22 spontaneous abortions; predominantly focal in 40% of 30 partial moles (33% mild atypia; 7% moderate-severe atypia); and, predominantly diffuse in 87% of 47 complete moles (21% mild atypia; 66% moderate-severe atypia). Among hydatidiform moles, the subsequent development of persistent gestational trophoblastic tumor did not relate to the degree of implantation site trophoblastic atypia. The authors conclude that trophoblast of the implantation site exhibits focal, mild atypia in some partial hydatidiform moles,and diffuse marked atypia in most complete hydatidiform moles. Thus, implantation site trophoblastic atypia may be a useful pathologic guideline regarding the diagnosis and classification of hydatidiform moles.

Abortion, Spontaneous↗
PubMed2006

Chemokine CXCL16, a scavenger receptor, induces proliferation and invasion of first-trimester human trophoblast cells in an autocrine manner.

BACKGROUND: The aim of this study was to investigate whether CXCL16/CXCR6, a newly identified chemokine pair, is expressed in first-trimester human placenta and whether they affect the trophoblast cell biology, since we have found CXCR6 highly transcribed in first-trimester human trophoblast cells previously. METHODS: We analysed the transcription and translation of CXCR6 and CXCL16 in purified first-trimester human trophoblast cells by real-time RT-PCR and immunochemical staining. We then examined the kinetic secretion of CXCL16 in the supernatant of primary-cultured trophoblast by enzyme-linked immunosorbent assay. We further investigated effects of CXCL16 on the proliferation and invasion of trophoblast cells in vitro. RESULTS: We found the chemokine pair CXCL16/CXCR6 was transcribed and translated in first-trimester trophoblast cells and JAR line. In addition, the primary-cultured trophoblasts secreted CXCL16 spontaneously and continuously in 100-h culture. Treating trophoblasts with CXCL16 induced marked proliferation and invasion in vitro. CONCLUSION: The findings from this study have demonstrated for the first time that CXCR6 and CXCL16 are co-expressed by first-trimester human trophoblast cells and stimulate their proliferation and invasion in an autocrine/paracrine manner. It suggests that CXCL16 plays important roles in human extravillous cytotrophoblast invasion and placentation.

Autocrine Communication↗
PubMed2000

Localization of E-cadherin in villous, extravillous and vascular trophoblasts during intrauterine, ectopic and molar pregnancy.

Previous reports have described down-regulation of E-cadherin in trophoblasts differentiating to an invasive phenotype. This study shows the localization of E-cadherin in a prospective design with stereological sampling of fetal and maternal first, second and third trimester tissue. E-cadherin was observed in villous cytotrophoblasts, and in non-proliferating, intermediate trophoblasts (IT) within cell columns and islands in intrauterine, ectopic and partial molar placentas. Highly proliferating IT with cytological atypia in complete molar placentas were also E-cadherin-positive. E-cadherin was present in trophoblasts throughout the anchoring cell columns. Trophoblasts undergoing epithelial mesenchymal transformation (EMT) detaching from the distal cell columns and deeper located single extravillous interstitial trophoblasts (EVT) showed E-cadherin-negative breaches in the cell membrane. Prior to the late second trimester, the relative number of E-cadherin-positive single EMT and EVT differed from the total number of cytokeratin-positive trophoblasts. Intraluminal, endovascular and perivascular trophoblasts adjacent to the maternal vessels were also E-cadherin-positive, but a highly varying pattern was observed at different ages of gestation. Our results indicate a temporary shift in E-cadherin expression in extravillous trophoblasts possessing a migrating and invasive potential. Functional E-cadherin may be restored as trophoblasts aggregate in the decidua and the vessel wall after completion of migration.

Antibodies, Monoclonal↗