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PubMed1988

[HLA-DP and HLA-DQ antigen expression on trophoblasts of normal human pregnancy and trophoblastic diseases].

A blocking antibody in pregnant sera seems essential in understanding why a fetus can survive as a semi-allograft in an immunologically competent mother. It has been demonstrated that blocking antibody is closely related to the paternal HLA-DR antigens. However, we previously reported that HLA-DR is not expressed on any trophoblast constituting the fetal frontier at the feto-maternal interface. The present study was then undertaken to clarify whether or not trophoblasts of normal pregnancy and trophoblastic diseases express HLA-DP or HLA-DQ antigens which are closely linked to HLA-DR as a haplotype. Materials were taken from ten pregnant uteri, ranging from 8 to 22 weeks of gestation, two uteri containing complete mole and two uteri each containing gestational choriocarcinoma. Curettage specimens obtained from three cases of complete mole and two cases of partial mole were also employed. Antigen expression was examined by an indirect immunoperoxidase technique using various monoclonal antibodies. From this immunohistochemical study, neither HLA-DP nor HLA-DQ seemed to be expressed on any trophoblast of normal pregnancy and trophoblastic diseases, which, together with the negative findings of HLA-DR on trophoblasts, may suggest that blocking antibody is not generated against HLA-D locus antigens on trophoblasts.

Female↗

PubMed1985

[Immunohistochemical study on trophoblast subpopulations in normal pregnancy and trophoblastic disease].

Trophoblast subpopulations were analyzed by their antigen expressions in normal pregnancy and trophoblastic disease. Samples were taken from uteri which were removed surgically. Frozen sections were stained by an avidin-biotin-peroxidase complex method, using monoclonal antibodies to HLA antigens and anti-Trop 1 antibody. Troma 1, a rat monoclonal antibody, was used for the identification of trophoblasts. The results were as follows: Troma 1 reacted with all trophoblasts specifically and could be used as a trophoblast marker in sections. HLA-A,B,C was negative on syncytiotrophoblast and villous cytotrophoblast but positive on nonvillous cytotrophoblast in normal pregnancy and hydatidiform mole. Some choriocarcinoma cells were positive for HLA-A,B,C and they were intermediate to large cytotrophoblast-like cells. No trophoblasts were positive for HLA-DR. Trop 1 was positive on villous cytotrophoblast in normal pregnancy and hydatidiform mole. Some choriocarcinoma cells were positive for Trop 1 and they were exclusively negative for HLA-A,B,C. From these immunohistochemical findings, trophoblasts of normal pregnancy and hydatidiform mole were divided into syncytiotrophoblast, villous cytotrophoblast, and nonvillous cytotrophoblast. Choriocarcinoma cells were classified into syncytiotrophoblast-like cells and three kinds of cytotrophoblast-like cells. They were analogous to those of normal pregnancy and hydatidiform mole to some extent, but a choriocarcinoma-specific subpopulation which was negative for HLA-A,B,C, HLA-DR, and Trop 1 was recognized.

Antibodies, Monoclonal↗

PubMed1986

[Reactivity of two monoclonal antibodies (Troma 1 and CAM 5.2) on tissue sections--as a histological trophoblast marker in normal pregnancy and trophoblastic disease].

In normal and molar pregnancy, non-villous trophoblasts which exist in the placental bed are thought to be difficult to be distinguished morphologically from the surrounding maternal cells. We examined the reactivities of two monoclonal antibodies (Troma 1 and CAM 5.2) by an immunoperoxidase technique and analyzed their usefulness as histological trophoblast markers. Materials were taken from 41 uteri of normal pregnancy, 7 uteri of hydatidiform mole, 2 uterine gestational choriocarcinoma, 1 tubal tissue of non-gestational choriocarcinoma and 5 non-gestational uteri. The reactivity of Troma 1 was observed on frozen sections and paraffin sections were employed in the analysis of CAM 5.2. The reactivities of these antibodies were the same. In nongestational tissue, they reacted with endometrial gland epithelia and endometrial covering epithelia. In placental bed of normal pregnancy, they reacted with villous and non-villous trophoblasts, besides endometrial gland epithelia. In molar sections, they reacted with gland epithelia, villous trophoblasts and also non-villous trophoblasts which proliferated towards maternal tissue. In choriocarcinoma, they reacted with carcinoma cells specifically. Since endometrial gland epithelia are easily identified histologically, it was concluded that these antibodies could work as histological trophoblast markers in normal pregnancy and trophoblastic disease.

Antibodies, Monoclonal↗

PubMed1989

Trophoblast differentiation during the transition from trophoblastic plate to lacunar stage of implantation in the rhesus monkey and human.

The transition from the trophoblastic plate stage to the early lacunar stage was examined in a series of implantation sites from the rhesus monkey, timed on the basis of the preovulatory estrogen peak, and prepared for transmission electron microscopy. This transition was compared with specimens from stage 5a, b, and c in the Carnegie collection of human embryos. The transition was marked by the differentiation of a new type of syncytial trophoblast--namely, a unilaminar microvillous polarized syncytium, which developed throughout the trophoblastic plate, forming characteristic intrasyncytial clefts. The rapid development of this type of syncytium created a nonclotting chamber for maternal blood wherever trophoblast intrusion into maternal vessels created confluence. Although the nature of the material in the Carnegie series precluded cytological characterization of the trophoblast, there is evidence that a similar transition occurs in human trophoblast and that in the human also the appearance of lacunae marks a change from an early invasive trophoblast to a situation in which growth is more significant.

Animals↗

PubMed1998

Reactivity of human trophoblast monoclonal antibodies with marmoset monkey trophoblast cultures.

The aim of this study was to determine whether cultured trophoblast tissues, derived from the trophectoderm of marmoset monkey blastocysts, contain homologues of human trophoblast antigens. This is an essential prerequisite to determine whether the marmoset may be a suitable model for preclinical testing of a human antitrophoblast antigen for fertility regulation. Previously evaluated monoclonal antibodies from the Flinders University laboratory, which reacted with human trophoblast with a high degree of specificity, were tested for immunohistochemical reactivity using an immunoperoxidase detection method on both frozen and paraformaldehyde-fixed sections of the cultured marmoset monkey trophoblast. All monoclonal antibodies raised against human placenta reacted positively, when compared to controls, suggesting that human and marmoset trophoblast cells share common epitopes. The specificity of the monoclonal antibodies was investigated by determining whether there was cross-reactivity with other marmoset monkey tissues, including adrenal, spleen, kidney, liver, muscle, ovary and testis. The specificities of the monoclonal antibodies on these marmoset tissues were similar to those previously found on the corresponding human tissues. We have concluded that marmoset monkey trophoblast exhibits homologues of human trophoblast antigens. The findings also suggest that marmoset monkeys should be evaluated further as a primate model to test suitable target antigens for antitrophoblast vaccines that may be useful contragestation agents in humans.

Animals↗

PubMed1996

Trophoblast proliferation rate does not predict progression to persistent gestational trophoblastic disease in complete hydatidiform mole.

Persistent gestational trophoblastic disease (PGTD) is a significant complication of complete hydatidiform mole. There are, however, no reliable clinical or pathological parameters to predict the development of PGTD following the evacuation of a complete mole. In this study we examined the value of Ki67 expression in the prediction of PGTD following complete mole. Immunohistochemistry for Ki67 was performed on 21 cases of complete mole complicated by PGTD and 17 cases that resolved spontaneously after evacuation. Strong Ki67 expression was seen in both villous cytotrophoblast and extravillous trophoblast of the complete moles. The Ki67 index of extravillous trophoblast was significantly higher than that of villous cytotrophoblast. There was no significant difference in Ki67 index of either villous cytotrophoblast or extravillous trophoblast between cases of complete mole complicated by PGTD and those that resolved spontaneously. Trophoblast proliferation rate does not predict outcome following complete hydatidiform mole. Other factors involved in myometrial invasion may be of importance in the development of this complication, but serum chorionic gonadotrophin level is the only reliable predictor of the development of persistent gestational trophoblastic disease.

Biomarkers↗

PubMed2026

Trophoblast Enrichment by Maternal Immune-Cell Depletion Using CD45 and CD56 Surface Markers in Trophoblast Retrieval and Isolation from the Cervix (TRIC).

Background: Trophoblast retrieval and isolation from the cervix (TRIC) has emerged as a promising alternative to invasive prenatal diagnostic procedures. However, contamination by maternal immune cells remains a major challenge that may compromise trophoblast purity and the reliability of downstream fetal genetic analyses. Methods: Maternal immune cells were selectively depleted by immunomagnetic sorting using antibodies targeting CD45 or CD56. The remaining cells were subsequently enriched for HLA-G-positive trophoblasts and characterized by immunofluorescence and gene-expression analyses using CD45, CD56, HLA-G, cytokeratin 7 (CK7), and β-human chorionic gonadotropin (β-hCG). Results: Compared with CD45-mediated depletion, CD56-mediated depletion demonstrated more efficient removal of maternal immune cells, as indicated by significantly reduced CD56 expression. CK7 expression showed an increasing trend following CD56 depletion, whereas β-hCG expression remained largely unchanged. Immunofluorescence analysis further demonstrated a significant increase in the proportion of CK7+/β-hCG+ trophoblast cells after CD56 depletion. Conclusions: Among the evaluated depletion strategies, CD56-mediated depletion demonstrated a more favorable profile for trophoblast-associated characteristics than CD45-mediated depletion, suggesting its potential contribution to further methodological optimization of trophoblast isolation in TRIC-based noninvasive prenatal genetic testing.

maternal immune cell↗

PubMedDate not supplied

Cytodifferentiation of trophoblast in the anchoring villi and trophoblastic shell in the first half of gestation in the macaque.

The structure of cytotrophoblast cells in cell columns of the anchoring villi and trophoblastic shell were studied by light and transmission electron microscopy during days 19-70 of pregnancy in the macaque. Additional placentas were prepared for 3H-thymidine autoradiography to demonstrate DNA synthesis. The cell columns of the anchoring villi consist of proximal, mid, and distal regions, and similarly the trophoblastic shell has a region forming the base of the intervillous space, a central zone, and a junctional zone. The proximal region of the cell column is composed of closely apposed, largely undifferentiated cytotrophoblast cells lacking intercellular space. In the mid region, the cells, which contain segregated glycogen areas, are separated into branching strands by extensive extracellular matrix. The distal zone abuts the trophoblastic shell and has fewer mostly peripheral cytotrophoblast cells and abundant matrix. Where cytotrophoblast of the shell is exposed to intervillous space or underlies syncytial trophoblast bordering the intervillous space, pads of cuboidal cells are seen. The central zone of the shell is arranged in strands of contiguous cells. Near the maternal junctional zone, the cells have fewer junctional regions and contain lipid rather than glycogen. Results of thymidine incorporation studies are consistent with observations of others using Ki67 distribution, indicating that cell replication occurs in the proximal region of the cell column, with subsequent migration of cells into the trophoblastic shell. Changes with age include an increase in extracellular matrix in the proximal region, a more linear organization in the expanded central zone of the shell, and a decrease in necrosis at the junction of the shell with endometrium, resulting in close association of shell cytotrophoblast cells, maternal decidual cells, large granular lymphocytes, and macrophages. It is concluded that the cytotrophoblast of the cell columns and trophoblastic shell is a pleomorphic cell type responding to adjacent constituents including the matrix it forms.

Animals↗

PubMed2000

Expression of cyclin E in placentas with hydropic change and gestational trophoblastic diseases: implications for the malignant transformation of trophoblasts.

BACKGROUND: Although much is known about the morphologic, cytogenetic, and clinical characters of gestational trophoblastic diseases, little information has appeared concerning the parameters related to their persistence or neoplastic transformation. Cell cycle alterations in tumor tissue were examined in this study in light of obvious changes in the clinical behavior of malignant cells. There is an increasing body of evidence suggesting that the abnormal expression of cyclins is considered one of the most important events in malignant transformation of various human cancers. Among these cell cycle regulators, the role of cyclin E in the neoplastic transformation of trophoblast populations has been poorly defined. METHODS: Using formalin fixed, paraffin embedded trophoblastic tissues, the authors investigated the expression of cyclin E by immunohistochemistry in placentas with hydropic change and gestational trophoblastic diseases. The specimens examined included tissue from 29 patients with complete hydatidiform mole, 18 patients with partial hydatidiform mole, and 6 patients with choriocarcinoma after term pregnancy or abortion. The authors also studied four cases of hydropic abortion. RESULTS: The cyclin E indexes (CEI) were as follows: 25.7% +/- 6.2% for hydropic change, 35.3% +/- 12.7% for triploid partial moles, 42.2% +/- 13.1% for diploid/tetraploid complete moles, and 63.6% +/- 9.5% for choriocarcinomas. There was a significant difference in CEI between placentas with hydropic change and partial mole (P = 0.04) and placentas with hydropic change and complete mole (P = 0.003). Choriocarcinomas had significantly higher cyclin E expression compared with placentas, partial moles, and complete moles, respectively. A significant correlation between the expression of cyclin E and S-phase fraction was observed in gestational trophoblastic diseases (rank correlation coefficient = 0.45, P < 0. 05). The relation between cyclin E expression and proliferation was abrogated in placentas with hydropic change, suggesting that cyclin E up-regulation represents a genuine aberration. CONCLUSIONS: The results of this study were consistent with the concept that cyclin E overaccumulation may play an important role in the uncontrolled proliferation and neoplastic transformation of trophoblasts.

Cell Cycle↗

PubMed1977

Development of radioimmunoassay for pregnancy-specific beta1-globulin and its measurement in serum of patients with trophoblastic and non-trophoblastic tumours.

Levels of human pregnancy-specific or trophoblast-specific beta1-globulin (TBG) were measured by double-antibody radioimmunoassay (RIA) in 103 patients with trophoblastic tumours and in 114 patients with a variety of non-trophoblastic tumours. The sensitivity of RIA for TBG was about 1 ng per ml. Twenty healthy adult females and males had levels below 1 ng per ml. Using the RIA for measurement of TBG in sera which were selected from immunodiffusion-TBG-negative samples, we detected elevated TBG levels in 76.7% of cases with trophoblastic tumours and in 15% of different cases with non-trophoblastic malignancies. The diagnostic and prognostic significance of the measurement of TBG levels by RIA in patients with trophoblastic tumours is discussed.

Adult↗

PubMed1987

Identification of extra-villous trophoblast cells in human decidua using an apparently unique murine monoclonal antibody to trophoblast.

Murine monoclonal antibodies were raised to human first trimester trophoblast cells. Eleven antibodies reacted with first trimester trophoblast, tested by immunoperoxidase staining on frozen sections, but only one had apparent specificity for trophoblast after examining reactivities with a panel of other cells and tissues. This antibody, designated FD0161G, bound selectively to syncytiotrophoblast and non-villous trophoblast in first trimester and term placentae. Villous cytotrophoblast was negative. This was clearly demonstrated on freeze-dried, paraffin embedded tissue sections which have superior architecture to frozen sections. FD0161G reacted with extra-villous trophoblast cells in human decidua which are also delineated by a monoclonal anti-cytokeratin antibody. Unlike the latter, however, FD0161G did not react with decidual glands. Thus FD0161G could be used as a specific probe for extra-villous trophoblast in decidual tissue.

Antibodies, Monoclonal↗

PubMed2005

Expression of serum amyloid A transcripts in human trophoblast and fetal-derived trophoblast-like choriocarcinoma cells.

The placenta comprises a highly specialized trophoblast layer, which arises from the embryo and differentiates during embryonic development to perform specialized functions, e.g., synthesis of pregnancy-associated hormones, growth factors and cytokines. As there is no evidence of maternal acute-phase protein transplacental transfer and trophoblast plays an important role in regulating immune responses at the feto-maternal interface, the expression of acute-phase serum amyloid A (A-SAA) was investigated in human first trimester trophoblast and trophoblast-like JAR and Jeg-3 choriocarcinoma cells. We here show expression of cytokine receptors and cytokine-dependent induction of A-SAA in JAR and Jeg-3 cells. While interleukin-1alpha/beta is a major agonist for A-SAA expression in JAR, tumor necrosis factor-alpha is the predominant agonist in Jeg-3. First trimester trophoblast and JAR/Jeg-3 cells further express the human homolog of SAA-activating factor-1, a transcription factor involved in cytokine-mediated induction of A-SAA genes. A-SAA1 and A-SAA2 transcripts were increased in first trimester trophoblast during pregnancy weeks 10 and 12 suggesting that A-SAA plays a role during early fetal development.

Cell Line, Tumor↗

PubMedDate not supplied

A trophoblast specific antigen, recognized by monoclonal antibody MA21, locates a unique trophoblast cell population in the murine placenta.

Monoclonal antibody MA21 recognized a 44kDa plasma membrane protein on F9 teratocarcinoma cells, trophectoderm of mouse peri-implantation-stage blastocyst and ectoplacental cone cells of 5 day postcoitum implanted blastocyst (Vernon, Linnemeyer and Hamilton, 1989). We show here that this antigen is expressed by trophoblast cells of the maturing placenta. Immunohistochemical assays of early and mature placental tissue sections, indirect immunofluorescence labelling of placental cultures and blastocyst outgrowths in vitro, and immunoprecipitation of 35S-labelled NP-40 extracts of placental cultures indicate the presence of a plasma membrane-associated antigen with the same characteristics as MA21 antigen of peri-implantation embryos and F9 teratocarcinoma cells. In sections of placentae, antigen-positive cells are always situated in a thin layer between trophoblastic giant cells and maternal tissue. In cultures of postimplantation stage embryos, attached trophoblast cells express MA21 antigen initially, but following transformation to the giant cell state, antigen is no longer expressed. These results indicate the presence of a plasma membrane protein antigen associated with a distinct population of cells believed to be trophoblast. We believe that these cells are the foremost trophoblast cells opposing maternal decidua and that they may give rise to secondary trophoblastic giant cells.

Animals↗

PubMedDate not supplied

Collagen phagocytosis by human extravillous trophoblast: potential role in trophoblastic invasion.

OBJECTIVES: To study collagen phagocytosis by human extravillous trophoblast. METHODS: First-trimester extravillous trophoblastic cell lines and primary trophoblast cell preparations were cultured in vitro with collagen-coated fluorescent latex beads and fluorescent-labeled collagen. Confocal microscopy was used to demonstrate internalization of collagen and beads. The effect of cytochalasin B, temperature, metabolic inhibitors, and cytokines was studied by culturing trophoblast cells with tritiated collagen. Acridine orange was used to stain for lysosomal compartments, and histochemical methods were used to demonstrate acid phosphatase in trophoblast cells. RESULTS: Both cell lines and primary culture cells internalize collagen and beads. Confocal microscopy unequivocally localized the phagocytosed material to the intracellular compartment. Inhibition by cytochalasin B and culture at 4C of uptake of [3H] collagen suggested that the process was phagocytosis. Cytokines and growth factors did not affect phagocytosis. Lysosomal compartments and acid phosphatase appear to colocalize. CONCLUSIONS: The continuous remodeling and turnover of collagen which occur in a wide variety of tissues under both physiologic and pathologic conditions are thought to be mediated by two pathways: one external (involving release of proteolytic enzymes), and the other internal (involving phagocytosis). Similar remodeling events are likely to occur during trophoblast invasion. Although current views emphasize the importance of the extracellular pathway, we postulate, on the basis of our findings, that both pathways are used, with the internal pathway probably being dominant. We hypothesize that the proteolytic enzymes (extracellular pathway) disrupt collagen matrices, thereby facilitating phagocytosis. It is teleologically sound to conceive of a dominant intracellular pathway, as it allows for more precise control of the process of invasion and is economical, as the products of collagen degradation can be used as energy sources or building blocks.

2,2'-Dipyridyl↗

PubMed1979

Antigens of human trophoblast. Effects of heterologous anti-trophoblast sera on lymphocyte responses in vitro.

This report describes the inhibition of human mixed lymphocyte culture (MLC) reactions by rabbit antisera to intact and detergent solubilized, fractionated, human trophoblast membranes. Heat-inactivated antisera were passed through solid-phase immunoabsorption columns of normal human serum and extensively absorbed with human erythrocytes, lymphocytes and liver powder. Immunohistological experiments with these absorbed antisera showed that they reacted brilliantly with syncytiotrophoblast in cryostat sections of human but not baboon or monkey placentae, and not with other normal adult tissues including peripheral blood lymphocytes (PBL). Addition of these antisera to MLC reactions produced significant and reproducible suppression of responses without affecting cell viability. Absorption studies demonstrated complete removal of MLC inhibition and trophoblast membranes but not with PBL or suspensions of HEp-2 cells. Timed experiments showed that optimal inhibition occurred when the antisera were added between 2 and 6 h after culture initiation, and that little suppression was achieved after 18 h. Lymphocytes harvested from MLC reactions after 2 h showed that 3--5% of the cells reacted with PBL/liver-absorbed anti-trophoblast sera, and that unstimulated PBL were negative. Cultures of subhuman primate lymphocytes in the presence of heterologous antisera to human trophoblast membranes showed total inhibition of rhesus:human and human:rhesus MLC, and no suppression of baboon:human or human:baboon reactions, whereas human lymphocytes responded in an exagerated manner when stimulated by baboon cells. Modulated MLC responses to human, rhesus, or baboon lymphocytes, in the presence of anti-trophoblast sera indicate that the antisera recognize trophoblast cross-reactive lymphocytes antigens. We propose that these antigens are reaction products of cell-cell interactions, and that the nature of the antigens is determined by the specificity of the recognition signals which initiate the reaction.

Animals↗

PubMed2005

PTHrP promotes murine secondary trophoblast giant cell differentiation through induction of endocycle, upregulation of giant-cell-promoting transcription factors and suppression of other trophoblast cell types.

The murine trophoblast cell lineage represents an intriguing experimental cell model as it is composed of four trophoblast stem (TS)-derived cell types: trophoblast giant cells (TGCs), spongiotrophoblast, syncytotrophoblast, and glycogen trophoblast cells. To investigate the role of parathyroid hormone-related protein (PTHrP) in TGC differentiation, we analyzed the effect of exogenous PTHrP on secondary TGCs of day 8.5 p.c. ectoplacental cone explant culture. Secondary TGCs expressed PTHrP and PTHR1 receptor in vivo and in vitro. TGCs treated with PTHrP had reduced proliferation and decreased apoptosis starting from day 2 in culture, and enhanced properties of giant cell differentiation: increased DNA synthesis, number of cells with giant nuclei and expression of placental lactogen-II (PL-II). The induction of TGC formation by PTHrP correlated with downregulation of cyclin B1 and mSNA expression, but upregulation of cyclin D1, thus allowing mitotic-endocycle transition. Moreover, PTHrP treatment influenced TGC differentiation by inducing the expression of transcription factors known to stimulate giant cell formation: Stra13 and AP-2gamma, and inhibiting the formation of other trophoblast cell types by suppressing trophoblast progenitors and spongiotrophoblast-promoting factors, Eomes, Mash-2, and mSNA. Taken together with the spatial and temporal patterns of TGC formation and PTHrP synthesis in vivo, these findings indicate an important role for PTHrP in the differentiation of secondary TGCs during placentation.

Animals↗

PubMed2005

ABC drug transporter expression and functional activity in trophoblast-like cell lines and differentiating primary trophoblast.

ATP-binding cassette (ABC) efflux transporters are expressed in the human placenta where they are thought to help protect the fetus from xenobiotics. To evaluate models for analysis of ABC transporter function and regulation in the placenta, we have characterized the expression and activity of multidrug resistance (MDR) 1/P glycoprotein (Pgp), MDR3/Pgp, breast cancer resistance protein (BCRP), and multidrug resistance proteins 1 and 2 (MRPs 1, 2) in differentiating primary trophoblast cells and BeWo and Jar cell lines. Real-time PCR and immunoblotting were used for analysis of mRNA and protein expression, respectively. Functional activity was measured using selective inhibitors of efflux of fluorescent substrates, calcein-AM (Pgp and MRPs) and Hoechst 33342 (BCRP). The levels of MDR1 mRNA and protein expression were much higher in trophoblast than in Jar and especially BeWo cells. Expression of MDR3 protein was also lower in BeWo cells. Levels of MDR3 expression were markedly higher than MDR1 levels in all tested cell types. Levels of both MDR1 and MDR3 expression decreased during trophoblast differentiation/syncytialization. BCRP was highly expressed in all cell types and increased with trophoblast differentiation. MRP1 expression was much lower in trophoblasts compared with both cell lines. In contrast to its abundant mRNA expression, MRP2 protein was practically undetectable in BeWo and Jar cells and was present only at very low levels in trophoblast. Functional studies confirmed the presence of active Pgp and BCRP in all studied cell types, whereas MRP functional activity was detected only in BeWo and Jar cells. Both cell lines may be useful models for studying various aspects of placental ABC transporter expression and function, but also have significant limitations. With respect to their ABC protein expression profile, Jar cells are more similar to nondifferentiated cytotrophoblast, whereas BeWo appear to more closely reflect differentiated syncytiotrophoblast.

ATP-Binding Cassette Transporters↗

PubMed2005

Platelet-derived soluble factors induce human extravillous trophoblast migration and differentiation: platelets are a possible regulator of trophoblast infiltration into maternal spiral arteries.

In early pregnancy, human extravillous trophoblasts (EVTs) invade and remodel maternal arteries. We have previously demonstrated that CCR1 is expressed on perivascular/endovascular trophoblasts and that CCR1 ligands promote EVT migration. In this study, we examined the physiologic roles of platelet-derived chemoattractants on EVT invasion. By immunohistochemistry, maternal platelets were localized among endovascular trophoblasts within the lumen of spiral arteries. Extracellular matrices (ECMs) were also detected among endovascular trophoblasts and platelets, suggesting that the platelets in these arteries were activated by ECMs. In vitro, platelets attached to EVTs isolated from human villous explant cultures and expressed P-selectin on the cell surface. Platelets significantly enhanced migration of EVTs without affecting proliferation of EVTs or secretion of MMP-2 or MMP-9. The invasion-enhancing effect of platelet-derived culture medium on EVTs was neutralized by anti-CCR1 antibody. Heat treatment completely abrogated the invasion-promoting effects of platelet-derived culture medium, but charcoal stripping did not. Platelets also induced endovascular trophoblast-like morphologic changes and integrin alpha1 expression in EVTs during 48-hour culture. These findings suggest that maternal platelets activated in the spiral arteries can regulate trophoblastic vascular infiltration and differentiation by releasing various soluble factors.

Arteries↗