Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “TROPHOBLAST”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed2004

High glucose levels down-regulate glucose transporter expression that correlates with increased oxidative stress in placental trophoblast cells in vitro.

OBJECTIVE: To study glucose transporter expression and oxidative stress in placental trophoblasts under hyperglycemic conditions in vitro. METHODS: Trophoblasts were isolated from term normal human placentas and incubated with Dulbecco's modified eagle medium containing 1000, 2500, and 4500 mg/L glucose for 3 days. At the end of incubation, culture medium was collected. Trophoblast RNA was extracted and mRNA expression of glucose transporters was determined by RNase protection assay. Messenger RNA expression for copper-zinc-superoxide dismutase (CuZn-SOD) was determined by real-time polymerase chain reaction. Lipid peroxide production was determined by measuring malondialdehyde concentration in the culture supernatant. Protein expression of sodium-glucose transporter 2 (SGLT-2) was determined by Western blot analysis. RESULTS: Messenger RNA expression for glucose transporter 1 (GLUT1) and SGLT-2 were reduced in trophoblast cells incubated with 4500 mg/L glucose compared with those incubated with 1000 and 2000 mg/L glucose. mRNA expression of CuZn-SOD was also decreased in trophoblasts incubated with 4500 mg/L glucose. Malondialdehyde production was significantly increased by trophoblasts incubated with 4500 mg/L glucose compared with those by trophoblasts incubated with 1000 and 2000 mg/L glucose (4.69 +/- 0.60 versus 2.10 +/- 0.29 and 2.89 +/- 0.47 nmol/mg protein; P < .01, respectively). CONCLUSIONS: Down-regulation of gene expression of glucose transporters correlates with increased lipid peroxide production and decreased superoxide dismutase expression in placental trophoblasts cultured under hyperglycemic conditions.

Cells, Cultured↗
PubMed2005

Microarray-based identification of differentially expressed genes in hypoxic term human trophoblasts and in placental villi of pregnancies with growth restricted fetuses.

Hypoxia adversely influences the function of the human placenta. We sought to identify a set of hypoxia-regulated transcripts in both term human trophoblasts in vitro and in villous trophoblasts in vivo. Using high-density oligonucleotide microarrays we initially examined differences in gene expression between trophoblast cultured in standard conditions (20% oxygen) vs. hypoxic conditions (< or =1% oxygen), as well as in placental tissues from pregnancies complicated by intrauterine growth restriction vs. matched controls. We used a novel computation method to compile data from the two approaches and identify transcripts that exhibited a marked expression change. Using quantitative PCR we confirmed an up-regulation of transcripts for vascular endothelial growth factor, connective tissue growth factor, follistatin-related protein, N-Myc down-regulated gene 1 and adipophilin in hypoxic term trophoblasts. In contrast, the expression of human placental lactogen and Beckwith-Wiedemann region 1 C was reduced in hypoxic trophoblast. Using in situ hybridization we validated the expression of each transcript in cultured term villous trophoblasts, and determined transcript expression in placental samples derived from four sets of dichorionic twins complicated by growth restriction of one twin. The identification of hypoxic trophoblast signature transcripts may implicate new mediators in pathways underlying trophoblast hypoxic injury and adaptation.

Base Sequence↗
PubMed2005

Expression of HERV-W Env glycoprotein (syncytin) in the extravillous trophoblast of first trimester human placenta.

Although the extravillous trophoblastic invasion has a critical role in human placental development, nothing is known about HERV-W expression in the extravillous phenotype. The aim of the present study was to localize in first trimester placenta the expression of HERV-W Env glycoprotein and its receptor all along the differentiation pathway of the extravillous phenotype. In addition using an in vitro model of extravillous cytotrophoblastic cell isolation and invasion we investigated the presence of HERV-W transcripts and envelope glycoprotein in cultured extravillous trophoblastic cells. Using monoclonal and polyclonal antibodies, the glycoprotein was immunolocalized in all the cell types of the extravillous phenotype lineage: cytotrophoblastic cells of the column, interstitial extravillous trophoblastic cells, multinucleated giant cells and endovascular trophoblast. Furthermore, using a polyclonal antibody, the D mammalian virus receptor was also localized in the various extravillous trophoblastic phenotypes. In addition, the presence of HERV-W transcripts and protein was demonstrated in cultured extravillous trophoblastic cells. HERV-W Env glycoprotein expressed in villous and extravillous trophoblast can be considered as a specific marker of the human trophoblast.

Adult↗
PubMed2005

Tissue-specific and ubiquitous basic helix-loop-helix transcription factors in human placental trophoblasts.

Tissue-specific class B basic helix-loop-helix (bHLH) transcription factors, dimerising with ubiquitously produced class A bHLH proteins, play a major role in murine trophoblast development. Here, we investigated expression patterns of class A and B bHLH factors in the human placenta and different trophoblast culture systems. Semi-quantitative RT-PCR and RNase protection assay revealed expression of the tissue-restricted factors Hash-2, I-mfa and Stra13 in placentae of early and late pregnancy, in purified villous trophoblasts as well as in invasive trophoblasts isolated from first trimester villous explant cultures. Accordingly, RNA in situ hybridisation localised Hash-2, I-mfa and Stra13 to the trophoblast epithelium, cell columns and extravillous trophoblasts invading maternal decidua. Villous stromal cells in situ and cultivated placental fibroblasts also produced I-mfa and Stra13 but failed to express Hash-2. The widely expressed class A proteins, E12/E47 were absent from all placental cell types while ITF-2 was restricted to placental stromal cells of early and late gestation. In contrast, HEB was identified in all trophoblast cell types using RT-PCR, Western blotting and immunohistochemistry. The negative HLH-regulators Id-1 and Id-2 lacking the DNA-binding domain, were detected in villous stromal cells and different cytotrophoblast subtypes but were absent from the syncytium. The data suggest that a complex interplay of activators (Hash-2, HEB) and repressors (Stra13, I-mfa) could be involved in extravillous trophoblast differentiation whereas downregulation of Id proteins could play a role in syncytialisation.

Adult↗
PubMed2006

Hypoxia regulates the expression of PHLDA2 in primary term human trophoblasts.

Hypoxia influences gene expression in placental trophoblasts. We sought to examine the effect of hypoxia on trophoblast expression of human PHLDA2 (also termed IPL, TSSC3 or BWR-1C), a product of an imprinted gene on human chromosome 11p15.5 whose murine ortholog plays a pivotal role in placental development. We initially confirmed that PHLDA2 was expressed in term placental villi, primarily in the trophoblast layer. Using quantitative PCR we found that the expression of PHLDA2 gradually declined during differentiation of primary term human trophoblasts. A similar expression pattern was seen for p57(Kip2) and IGF-II, both products of imprinted genes on chromosome 11p15.5. Exposure of trophoblasts to hypoxia in vitro (O(2)<or=2%) markedly reduced the expression of PHLDA2 mRNA and protein. This effect was not consistent among other chromosome 11p15.5 genes products, as the expression of p57(Kip2) decreased, but that of IGF-II increased in hypoxic trophoblasts. PHLDA2 expression in trophoblasts exposed to TGFbeta1, -beta2 or -beta3 was unchanged. We conclude that hypoxia down-regulates the expression of PHLDA2 in human term placental trophoblasts. As murine PHLDA2 limits placental growth, our results suggest that down-regulation of PHLDA2 attenuates the impact of hypoxia on placental growth.

Cells, Cultured↗
PubMed1992

The fetus as an allograft: immunobiologic role of human trophoblasts for fetal survival.

OBJECTIVE: The hypothesis of this study is that trophoblasts contribute to the survival of the mammalian fetal allograft. STUDY DESIGN: Immunologic and molecular biologic studies were performed with human trophoblasts or trophoblastic tumor cells to investigate the expression of class I human leukocyte antigens, the susceptibility to natural killer and lymphokine-activated cells, the ontogeny of Fc gamma-receptors, and the production of immunosuppressive factors. RESULTS: Heterogeneous expression of class I human leukocyte antigens on trophoblasts was regulated at transcriptional level. Trophoblasts showed low susceptibility to natural killer and lymphokine-activated cells. Trophoblasts expressed natural killer cell-type Fc gamma-receptor III, which mediates phagocytosis. The trophoblast-derived immunosuppressive factor was very similar to transforming growth factor-beta. CONCLUSION: The trophoblasts, which ultimately form the fetoplacental interface, constitute a major immune barrier for the survival of the allogenic conceptus.

Female↗
PubMed2002

Human cytomegalovirus-caused damage to placental trophoblasts mediated by immediate-early gene-induced tumor necrosis factor-alpha.

Infection of the fetal epithelium (trophoblast) lining the villous placenta by human cytomegalovirus (HCMV) accompanies placental inflammations and fetal intrauterine growth restriction. However, the consequences of infection on the villous trophoblast have not been explored. We show that HCMV infection of primary immature (cytotrophoblast-like) or mature (syncytiotrophoblast-like) cultures results in loss of half of the cells within 24 hours of virus challenge. Two-color immunofluorescence of HCMV immediate early (IE) gene expression and apoptosis (terminal dUTP nick-end labeling) revealed apoptosis only in uninfected cells. Antibody to tumor necrosis factor (TNF)-alpha completely inhibited infection-induced trophoblast apoptosis and cell loss, as did co-incubation with epidermal growth factor, known to inhibit trophoblast apoptosis. Transfection with HCMV immediate early- (IE)1-72 and IE2-86, but not IE2-55, expression plasmids induced paracrine trophoblast apoptosis inhibitable by epidermal growth factor or antibody to TNF-alpha. These results show that HCMV infection of villous trophoblasts leads to rapid loss of neighboring cells mediated by viral IE protein-induced TNF-alpha secretion. We propose that HCMV infection damages the placental trophoblast barrier by accelerating trophoblast turnover and decreasing its capacity for renewal.

Apoptosis↗
PubMed1977

Gestational trophoblastic neoplasms: morphologic considerations.

Abnormal trophoblastic proliferation is the hallmark of a spectrum of lesions constituting the gestational trophoblastic neoplasms. Rapid proliferation, infiltration, vascular invasion, hematogenous dissemination, and spontaneous regression are features of both normal and neoplastic trophoblast. Trophoblastic hyperplasia without hydrops, hydatidiform mole, invasive mole, and gestational choriocarcinoma are related lesions, characterized by increasingly aberrant trophoblastic growth and worsening prognosis, if untreated. Difficulties in diagnosis may arise with respect to the normal early implantation site, the hydropic abortus, and postgestational, involuting, residual trophoblast. Histologic grading or hydatidiform moles is relevant to their prognosis and biologic behavior. Trophoblastic neoplasia may begin at any stage of pregnancy or puerperally with immediate or late and local or distant manifestations in the mother or the child. Cognizance of the capricius potential behavior of trophoblast permits successful management of its proliferative lesions, monitored by serial measurement of gonadotropin secretion.

Choriocarcinoma↗
PubMed2004

Differentiation of placental trophoblast giant cells requires downregulation of p53 and Rb.

Trophoblast giant cells in the rodent placenta form the outermost layer of the extraembryonic compartment, establish direct contact with maternal cells, and produce a number of pregnancy-specific cytokine hormones. Giant cells differentiate from proliferative trophoblasts as they exit the cell cycle and enter a genome-amplifying endocycle, a process we show involves decreased expression of the G1 checkpoint proteins p53 and Rb. Although p53 mRNA levels are unchanged in proliferative compared to differentiated trophoblasts, p53 protein levels are markedly reduced in giant cells. Forced expression of wild type p53 in trophoblasts inhibits differentiation, and expression of a dominant negative p53 peptide stimulates differentiation. Consistent with the loss of p53 protein, differentiated trophoblasts become resistant to apoptosis-inducing agents. Decreased expression of Rb is also detected during differentiation, and overexpression of Rb in trophoblasts inhibits giant cell differentiation. Although an increase in E2F activity would be expected with the loss of Rb, what is observed is an overall decrease in E2F DNA-binding complexes, a shift to new complexes, and a decrease in E2F-dependent gene expression in differentiating trophoblasts. Overall, these results indicate that the combination of a decrease in p53 and Rb represents a functionally important part of the transition of trophoblasts from a proliferative cell cycle to an endocycle in the giant cell differentiation programme.

Animals↗
PubMedDate not supplied

Review article: trophoblast invasion and the establishment of haemochorial placentation in man and laboratory animals.

Trophoblast invasion is an essential component of haemochorial placentation and has to be considered to relation to reactive changes in the maternal uterine tissues. Some comparative aspects of human and laboratory rodents are discussed and, although there is an obvious phylogenetic gap between the two, many characteristics of placental development are found to be analogous. Trophoblast growth into the uterus is different in different species: localized trophoblast growth forming a bulky tissue (mouse, rat, hamster) contrast with a dispersion of independent trophoblastic elements, forming an interstitial invasion (guinea pig, man). In the rat, mouse, hamster and man retrograde intra-arterial trophoblast migration occurs in maternal vessels supplying blood to the developing placenta. Early changes in maternal tissue might influence trophoblast behaviour. Decidualization probably is a key phenomenon, and the relation of decidual necrosis to trophoblast invasion is considered. Some kind of controlled immune response by the mother also may be involved. These considerations apply to stromal or interstitial invasion as well as to intravascular trophoblast migration but, for the latter, haemodynamic factors probably influence tissue reactions.

Adaptation, Physiological↗
PubMed1998

Expression and localization of membrane type matrix metalloproteinase-1 (MT1-MMP) in trophoblast cells of cultured mouse blastocysts and ectoplacental cones.

Membrane type matrix metalloproteinases (MT-MMPs) possess a C-terminal transmembrane domain and are expressed on the cell membrane. It was suspected, therefore, that MT1-MMP might play an important role in the trophoblastic invasion during implantation. The patterns of expression and localization of membrane type matrix metalloproteinase-1 (MT1-MMP) were examined immunocytochemically in cultured mouse blastocysts and excised extoplacental cones (EPCs). MT1-MMP immuno-reactivity was present in the giant trophoblast cells located at the periphery of the spreading trophoblast of cultured blastocysts and the outgrowths of cultured EPCs, but not in the densely packed trophoblast cells in both the blastocysts and the EPCs. It appears likely that MT1-MMP expressed on the edge of the invading trophoblast facilitates the trophoblastic invasion by cleaving proMMP-2, a known substrate of MT1-MMP, in the decidua. Immunohistochemical examination of early conceptuses confirmed that the trophoblast cells actively invading the endometrium in vivo express MT1-MMP strongly. It is suggested, furthermore, that the expression of MT1-MMP might be downregulated by cell-cell contact in mouse trophoblast cells, as in the mouse mammary epithelial cell line HC11.

Animals↗
PubMed2002

Effect of shear stress on migration and integrin expression in macaque trophoblast cells.

During fetal development, trophoblast cells enter endometrial capillaries, migrate within the uterine vasculature, and eventually reside within spiral arteries of the uterus. This invasive activity is accompanied by upregulation of trophoblast beta1 integrin expression. Fluid mechanical shear stress regulates migration and expression of adhesion molecules in vascular endothelial cells, but nothing is known about the effects of shear stress on trophoblast cells. We tested the hypothesis that shear stress regulates the motility and beta1 integrin expression of trophoblast cells. Early gestation macaque trophoblast cells were cultured in 1 x 1-mm square cross-section capillary tubes within which the flow field was determined using three-dimensional computational fluid dynamic simulations. Trophoblast cells in the capillary tubes were exposed to a steady shear stress of 7.5, 15, or 30 dyn/cm2 for up to 24 h. In the absence of flow, trophoblast cells were highly dynamic with constant nondirectional positional shifts but with no net cell migration. Exposure of the cells to shear stress within 24-72 h of cell plating significantly increased the level of this activity and led to net cell migration in the direction of flow. Shear stress also increased the expression and altered the topography of beta1 integrin. These results suggest that shear stress regulates trophoblast motility and beta1 integrin expression in vitro.

Animals↗
PubMed1999

Vitronectin receptors are expressed by macaque trophoblast cells and play a role in migration and adhesion to endothelium.

The objective of this work was to develop an in vitro system that would extend the usefulness of the macaque as a model for studying trophoblast invasion and spiral artery modification. We sought to determine whether trophoblast cells isolated from early gestation macaque placentas expressed vitronectin receptors and tested the idea that these receptors play a role in trophoblast migration and adhesion. Cytotrophoblast cells were isolated from 40-100 day macaque placentas, cultured, and characterized by immunofluorescence microscopy and flow cytometry. The cells expressed alphaV, beta3, and beta1 integrins on their surfaces. Immunohistochemical analysis of early gestation placentas and decidua basalis confirmed that intravascular trophoblast cells express alphaVbeta3/beta5. Using migration chambers we found that the trophoblast cells migrated towards vitronectin but not towards bovine serum albumin. This specific migration was blocked by preincubating the trophoblast cells with anti-vitronectin receptor (alphaVbeta3/beta5) antibodies. In other experiments, macaque trophoblast cells adhered to myometrial endothelial cells in a time-dependent manner and adhesion was significantly blocked by antibodies against alphaVbeta3/beta5 integrin. The results suggest that vitronectin receptors expressed by macaque trophoblast cells play a role in the migratory activity of these cells and may also be important in mediating attachment to endothelium.

Animals↗
PubMed2001

Macrophage-induced apoptosis limits endovascular trophoblast invasion in the uterine wall of preeclamptic women.

Impaired invasion of uteroplacental arteries by extravillous trophoblast cells is a key pathogenic mechanism of preeclampsia. We previously demonstrated that reduced trophoblast invasion into uteroplacental spiral arteries was associated with an excess of macrophages in and around these arteries. To explore the significance of these observations, we correlated the extent of extravillous trophoblast apoptosis in placental bed biopsy specimens with macrophage distribution and studied the effect of macrophages upon trophoblast apoptosis in vitro. Extravillous trophoblast hybrid cells were cocultured with activated macrophages exposed to exogenous tumor necrosis factor alpha (TNFalpha), anti-tumor necrosis factor receptor I (TNF-RI), and tryptophan depletion, and the rates of trophoblast apoptosis were measured. Extravillous trophoblast hybrid cells showed increased rates of apoptosis following exposure to exogenous TNFalpha, with tryptophan depletion, and when cocultured with activated macrophages. The proapoptotic effects of macrophages in vitro were completely inhibited only by simultaneous addition of tryptophan and anti-TNF-RI. Our data indicate that macrophages, residing in excess in the placental bed of preeclamptic women, are able to limit extravillous trophoblast invasion of spiral arterial segments through apoptosis mediated by the combination of TNFalpha secretion and tryptophan depletion. The mechanisms by which macrophages are activated and recruited to the placental bed are presently unknown but are likely central to the pathogenesis of preeclampsia.

Adult↗
PubMed1999

Expression of CD1D mRNA transcripts in human choriocarcinoma cell lines and placentally derived trophoblast cells.

Human placental trophoblast is critically involved in mediating maternal tolerance of the fetal semiallograft. Genes encoding highly polymorphic major histocompatibility complex (MHC) class I and class II antigens that could provoke maternal immune rejection responses are silenced in trophoblast. However, several MHC class I or class I-related products exhibiting reduced or negligible polymorphism are expressed and assumed to be functionally involved in maintaining pregnancy. The CD1 gene family encodes non-polymorphic MHC class I-like products that have the unusual ability to present non-peptide antigens to T cells. One member, CD1D, is expressed in certain epithelial cells and interacts with a specific T-cell subset that may promote the development of Th2-mediated responses believed to be associated with pregnancy. In this study we examined the expression of CD1D in human trophoblast cell lines and placentally derived trophoblast cells by reverse transcriptase-polymerase chain reaction using CD1D-specific oligonucleotide primers. We have found that CD1D mRNA transcripts are expressed in trophoblast cells and cell lines. We have also identified a novel alternatively spliced CD1D mRNA transcript lacking exon 4. Exon 4-intact and exon 4-deficient CD1D transcripts appear to be differentially expressed in different trophoblast and non-trophoblast cell populations. Our studies suggest that at least one member of the CD1 family is transcribed in human trophoblast.

Antigens, CD1↗
PubMed2001

Polyploidization in the trophoblast and uterine glandular epithelium of the endotheliochorial placenta of silver fox (Vulpes fulvus Desm.), as revealed by the DNA content.

Dynamics of genome multiplication during establishment of interrelations between trophoblast and glandular epithelium of the endometrium has been studied in the course of formation of placenta in the silver fox. During formation of the placenta, penetration of the trophoblast into the zone of the endometrial glandular epithelium and of endometrial blood vessels into the zone of expanding trophoblast occurs. The trophoblast, which gradually replaces epithelium and a part of the stroma of the endometrium, closely adjoins endometrial vessels but does not disrupt them, thereby the endotheliochorial placenta is formed. Cytophotometric measurements of the DNA content in trophoblast nuclei have shown that most of them are polyploid: predominantly 4-64c, occasionally 128c and 256c. Polyploidy of the trophoblast may be a consequence of various types of polyploidizing mitoses. Cytophotometric measurements of the DNA content in mitotic figures have revealed the presence of mitoses of diploid cells, i.e. with the DNA amount of 4c (2n), and polyploid cells, i.e. 8c (4n), and 16c (8n), therefore trophoblast cells in the silver fox placenta are able to enter mitosis up to the octaploid level. Higher degrees of polyploidy in the trophoblast cells seem to be achieved by endoreduplication. Polyploidization of the uterine glandular epithelial cells during placentation in the silver fox occurs until the level of 8c. Thus, the tissue-specific response of the uterus to the implanting embryo consists of active proliferation and polyploidization of the glandular epithelium, which may compensate formation of prominent population of decidual cells (i.e., connective tissue cells). In the endotheliochorial placenta of the silver fox the regularity is confirmed that cells of both maternal and fetal origin are, as a rule, polyploid in sites of their contact in placenta, which may be of protective significance in the contact of allogenic organisms.

Animals↗
PubMedDate not supplied

Inconsistency of fetal trophoblast cells in first trimester maternal peripheral blood prevents non-invasive fetal testing using this cell target.

We have investigated whether maternal peripheral blood from the first trimester of pregnancy is a reliable source of identifiable trophoblast cells. The cells were enriched from 30 ml of venous blood, with multiple antibodies shown previously to enrich trophoblasts and a new cocktail based on known trophoblast surface features. Three different magnetic solid phases were tested to enrich trophoblasts, and both positive and negative cell enrichment strategies were examined. The cells were identified as trophoblast by morphology coupled with immunocytochemistry to co-localize cytokeratin with one of three IGF-II, PAI-1 or hPLH proteins or by in-situ hybridization with a mixture of 50 oligos directed to eight different expressed genes, alpha-HCG, IGF-II, PAI-1, HASH2, hPLH, p57(KIP2), PP5, H-19. While these tools worked beautifully in chorionic villi cell/sprout preparations and tissue sections, we could not detect and identify any trophoblasts in maternal peripheral blood even if the maternal peripheral blood was drawn 5-20 min following termination of pregnancy or from individuals maintaining the pregnancy. Based on our own experience and that of some reports in the literature, trophoblasts do not appear to be a viable candidate for fetal screening using maternal peripheral blood as the source. It is important to note that while trophoblast deportation is a biological phenomenon that has been described repeatable, they do not provide a means to perform prenatal genetic diagnosis.

Antibodies↗
PubMed2003

Regulatory transcription factors controlling function and differentiation of human trophoblast--a review.

In transgenic mice, homozygous mutations of trophoblast-specific transcription factors such as Hand1, Mash-2, I-mfa or GCM1 revealed their key regulatory roles in induction, maintenance or differentiation of distinct placental trophoblast subpopulations in vivo. Descriptive studies have shown that several of these factors are also expressed in the human placenta, suggesting that the molecular mechanisms governing trophoblast differentiation could be similar in mice and men. While an increasing number of putative developmental regulators are being identified in the human placenta, little information is available regarding whether the particular factors play an essential role in trophoblast differentiation processes such as formation of anchoring villi, placental bed invasion or syncytialization. However, expression of abundant trophoblast-specific products such as hormones can be regarded as a hallmark of differentiation, suggesting that the factors controlling their transcription could also be involved in the developmental processes of the placenta. Indeed, studies in different model systems revealed that the human homologues of murine trophoblast-specific transcriptional regulators interact with the promoter regions of typical placental genes such as aromatase P450 (CYP19), chorionic gonadotrophin (CG) or placental lactogen (PL). Additionally, the unique combination of more broadly distributed transcription factors of the Sp or Ap-2 protein family in a particular trophoblast cell type is required to govern mRNA expression in a differentiation-dependent manner. Here, we will summarize our present knowledge on these individual transcription factors that are involved in human trophoblast function and differentiation.

Animals↗