Journal articles: 'Syncytiotrophoblasts'

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McConkey, Cameron A., Elizabeth Delorme-Axford, Cheryl A. Nickerson, Kwang Sik Kim, Yoel Sadovsky, Jon P. Boyle, and Carolyn B. Coyne. "A three-dimensional culture system recapitulates placental syncytiotrophoblast development and microbial resistance." Science Advances 2, no. 3 (March 2016): e1501462. http://dx.doi.org/10.1126/sciadv.1501462.

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In eutherians, the placenta acts as a barrier and conduit at the maternal-fetal interface. Syncytiotrophoblasts, the multinucleated cells that cover the placental villous tree surfaces of the human placenta, are directly bathed in maternal blood and are formed by the fusion of progenitor cytotrophoblasts that underlie them. Despite their crucial role in fetal protection, many of the events that govern trophoblast fusion and protection from microbial infection are unknown. We describe a three-dimensional (3D)–based culture model using human JEG-3 trophoblast cells that develop syncytiotrophoblast phenotypes when cocultured with human microvascular endothelial cells. JEG-3 cells cultured in this system exhibit enhanced fusogenic activity and morphological and secretory activities strikingly similar to those of primary human syncytiotrophoblasts. RNASeq analyses extend the observed functional similarities to the transcriptome, where we observed significant overlap between syncytiotrophoblast-specific genes and 3D JEG-3 cultures. Furthermore, JEG-3 cells cultured in 3D are resistant to infection by viruses and Toxoplasma gondii, which mimics the high resistance of syncytiotrophoblasts to microbial infections in vivo. Given that this system is genetically manipulatable, it provides a new platform to dissect the mechanisms involved in syncytiotrophoblast development and microbial resistance.

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Hemmings, D. G., R. Kilani, C. Nykiforuk, J. Preiksaitis, and L. J. Guilbert. "Permissive Cytomegalovirus Infection of Primary Villous Term and First Trimester Trophoblasts." Journal of Virology 72, no. 6 (June 1, 1998): 4970–79. http://dx.doi.org/10.1128/jvi.72.6.4970-4979.1998.

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ABSTRACT Forty percent of women with primary cytomegalovirus (CMV) infections during pregnancy infect their fetuses with complications for the baby varying from mild to severe. How CMV crosses the syncytiotrophoblast, the barrier between maternal blood and fetal tissue in the villous placenta, is unknown. Virus may cross by infection of maternal cells that pass through physical breaches in the syncytiotrophoblast or by direct infection of the syncytiotrophoblast, with subsequent transmission to underlying fetal placental cells. In this study, we show that pure (>99.99%), long-term and healthy (>3 weeks) cultures of syncytiotrophoblasts are permissively infected with CMV. Greater than 99% of infectious progeny virus remained cell associated throughout culture periods up to 3 weeks. Infection of term trophoblasts required a higher virus inoculum, was less efficient, and progressed more slowly than parallel infections of placental and human embryonic lung fibroblasts. Three laboratory strains (AD169, Towne, and Davis) and a clinical isolate from a congenitally infected infant all permissively infected trophoblasts, although infection efficiencies varied. The infection of first trimester syncytiotrophoblasts with strain AD169 occurred at higher frequency and progressed more rapidly than infection of term cells but less efficiently and rapidly than infection of fibroblasts. These results show that villous syncytiotrophoblasts can be permissively infected by CMV but that the infection requires high virus titers and proceeds slowly and that progeny virus remains predominantly cell associated.

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H K, Sharath Kumar, Chaitra N, Nataraju G, and Bharathi M. "Immunohistochemical Study of VEGF in Placenta of Hypertensive Mothers." Annals of Pathology and Laboratory Medicine 7, no. 9 (September 25, 2020): A474–477. http://dx.doi.org/10.21276/apalm.2834.

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Background: Pregnancy is most commonly complicated by Hypertensive disorders. In India, the incidence of gestational hypertension varies from 0.5-1.8%. VEGF is a prime regulator of angiogenesis and overall maintenance of endothelial cell health. This study aims to determine the role of VEGF in placentae of Hypertensive and Normotensive pregnancies by assessing its immunohistochemical expression in Syncytiotrophoblasts. Methods: The study was conducted in the Department of Pathology in our institute. This is a case-control study which included 50 placentae. Out of which,25 were from Normal mothers and 25 placentae from Hypertensive mothers. Immunohistochemistry for VEGF was performed on tissue section using commercially available monoclonal antibodies. The results were interpreted by evaluating Positivity and Intensity of Immunostaining. Result: Out of 25 Hypertensive placentae, 22 showed Positivity for VEGF immunostaining. Out of 25 Normotensive placentae, 23 showed Negative results for syncytiotrophoblastic staining of VEGF. The difference in VEGF expression in syncytiotrophoblast of hypertensive and normotensive placentae was statistically significant. Conclusion: Hypoxia acts as a potent stimulus for induction of VEGF mRNA in an attempt to normalize fetal blood flow and thus VEGF is increased. This results in the notable increase in immunohistochemical expression of VEGF in the syncytiotrophoblasts of hypertensive placenta.

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Longtine, Mark S., Silvija Cvitic, Bryanne N. Colvin, Baosheng Chen, Gernot Desoye, and D. Michael Nelson. "Calcitriol regulates immune genes CD14 and CD180 to modulate LPS responses in human trophoblasts." Reproduction 154, no. 6 (December 2017): 735–44. http://dx.doi.org/10.1530/rep-17-0183.

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We assessed the response of primary cultures of placental villous mononucleated trophoblasts and multinucleated syncytiotrophoblast to calcitriol, the most biologically active form of vitamin D. Whole-genome microarray data showed that calcitriol modulates the expression of many genes in trophoblasts within 6 hours of exposure and RT-qPCR revealed similar responses in cytotrophoblasts, syncytiotrophoblasts and villous explants. Both cytotrophoblasts and syncytiotrophoblasts expressed genes for the vitamin D receptor, for LRP2 and CUBN that mediate internalization of calcidiol, forCYP27B1that encodes the enzyme that converts calcidiol into active calcitriol, and forCYP24A1that encodes the enzyme that modifies calcitriol and calcidiol to inactive calcitetrol. Notably, we found an inverse effect of calcitriol on expression of CD14 and CD180/RP105, proteins that differentially regulate toll-like receptor 4-mediated immune responses. Supported by gene ontology analysis, we tested the hypothesis that CD14 and CD180 modulate the inflammatory response of syncytiotrophoblast to bacterial lipopolysaccharide (LPS). These cells showed a robust response to a wide range of LPS concentrations, with induction of active NF-κB and increased secretion of IL-6 and IL-8. SiRNA-mediated knockdown ofCD14reduced the secretion of IL-6 and IL-8 in response to LPS. Collectively, our data showed that calcitriol has a rapid and widespread effect on villous trophoblast gene expression in general, and a specific effect on the innate immune response by syncytiotrophoblast.

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Lacroux, C., F. Corbière, G. Tabouret, S. Lugan, P. Costes, J. Mathey, J. M. Delmas, et al. "Dynamics and genetics of PrPSc placental accumulation in sheep." Journal of General Virology 88, no. 3 (March 1, 2007): 1056–61. http://dx.doi.org/10.1099/vir.0.82218-0.

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Placentae from scrapie-affected ewes are an important source of contamination. This study confirmed that scrapie-incubating ewes bearing susceptible genotypes could produce both abnormal prion protein (PrPSc)-positive and -negative placentae, depending only on the PRP genotype of the fetus. The results also provided evidence indicating that scrapie-incubating ARR/VRQ ewes may be unable to accumulate prions in the placenta, whatever the genotype of their progeny. Multinucleated trophoblast cells appeared to play a key role in placental PrPSc accumulation. PrPSc accumulation began in syncytiotrophoblasts before disseminating to uninucleated trophoblasts. As these result from trophoblast/uterine epithelial cell fusion, syncytiotrophoblast cells expressed maternal and fetal PrPC, whilst uninucleated trophoblast cells only expressed fetal PrPC. In ARR/VRQ scrapie-infected ewes, expression of the ARR allele by syncytiotrophoblasts appeared to prevent initiation of PrPSc placental deposition. The absence of prions in affected ARR/VRQ sheep placentae reinforces strongly the interest in ARR selection for scrapie control.

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Colvin, Bryanne N., Mark S. Longtine, Baosheng Chen, Maria Laura Costa, and D. Michael Nelson. "Oleate attenuates palmitate-induced endoplasmic reticulum stress and apoptosis in placental trophoblasts." Reproduction 153, no. 4 (April 2017): 369–80. http://dx.doi.org/10.1530/rep-16-0576.

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Pre-pregnancy obesity is increasingly common and predisposes pregnant women and offspring to gestational diabetes, pre-eclampsia, fetal growth abnormalities and stillbirth. Obese women exhibit elevated levels of the two most common dietary fatty acids, palmitate and oleate, and the maternal blood containing these nutrients bathes the surface of trophoblasts of placental villi in vivo. We test the hypothesis that the composition and concentration of free fatty acids modulate viability and function of primary human villous trophoblasts in culture. We found that palmitate increases syncytiotrophoblast death, specifically by caspase-mediated apoptosis, whereas oleate does not cause enhanced cell death. Importantly, exposure to both fatty acids in equimolar amounts yielded no increase in death or apoptosis, suggesting that oleate can protect syncytiotrophoblasts from palmitate-induced death. We further found that palmitate, but not oleate or oleate with palmitate, increases endoplasmic reticulum (ER) stress, signaling through the unfolded protein response, and yielding CHOP-mediated induction of apoptosis. Finally, we show that oleate or oleate plus palmitate both lead to increased lipid droplets in syncytiotrophoblasts, whereas palmitate does not. The data show palmitate is toxic to human syncytiotrophoblasts, through the induction of ER stress and apoptosis mediated by CHOP, whereas oleate is not toxic, abrogates palmitate toxicity and induces fat accumulation. We speculate that our in vitro results offer pathways by which the metabolic milieu of the obese pregnant woman can yield villous trophoblast dysfunction and sub-optimal placental function.

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Chen, Baosheng, Mark S. Longtine, Yoel Sadovsky, and D. Michael Nelson. "Hypoxia downregulates p53 but induces apoptosis and enhances expression of BAD in cultures of human syncytiotrophoblasts." American Journal of Physiology-Cell Physiology 299, no. 5 (November 2010): C968—C976. http://dx.doi.org/10.1152/ajpcell.00154.2010.

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Hypoxia is commonly assigned a role in the placental dysfunction characteristic of preeclampsia and intrauterine growth restriction. We previously showed that hypoxia upregulates p53 and enhances apoptosis in primary cultures of human cytotrophoblasts. Here we tested the hypothesis that hypoxia also induces apoptosis in syncytiotrophoblasts by upregulation of p53. Primary cultures of human cytotrophoblasts that had differentiated into syncytiotrophoblasts by 52 h were exposed for ≤24 h to 20% or <1% oxygen in the presence or absence of staurosporine or the p53 modulators nutlin-3, pifithrin-α, and pifithrin-μ. Proteins were detected by Western blot analysis or immunofluorescence. Compared with 20% oxygen, exposure of syncytiotrophoblasts to <1% oxygen upregulated hypoxia-inducible factor (HIF)-1α and rapidly downregulated p53. Activity of p53 in hypoxic syncytiotrophoblasts was reduced by the higher expression of the negative p53 regulator MDMX and by the reduction of phosphorylation of p53 at Ser392, which reduces p53 activity. Conversely, staurosporine, a kinase inhibitor, and nutlin-3, a drug that enhances p53 expression, both raised p53 levels and increased the rate of apoptosis in syncytiotrophoblasts compared with vehicle controls. Immunofluorescence staining showed p53 immunolocalized to both cytoplasm and nuclei of nutlin-3-exposed syncytiotrophoblasts. The hypoxia-induced apoptosis in syncytiotrophoblasts correlated with enhanced expression of the proapoptotic BAD and a reduced level of antiapoptotic BAD phosphorylated on Ser112. We surmise that cell death induced by extreme hypoxia in syncytiotrophoblasts follows a non-p53-dependent pathway, unlike that of a nonhypoxic stimulus and unlike hypoxic cytotrophoblasts. We speculate that downregulation of p53 activity in response to hypoxia reduces or eliminates the apoptosis transduced by the p53 pathway in syncytiotrophoblasts, thereby limiting cell death and maintaining the integrity of this critical villous component.

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Wang, Ying, Baosheng Chen, Mark S. Longtine, and D. Michael Nelson. "Punicalagin promotes autophagy to protect primary human syncytiotrophoblasts from apoptosis." REPRODUCTION 151, no. 2 (February 2016): 97–104. http://dx.doi.org/10.1530/rep-15-0287.

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Punicalagin is a prominent polyphenol in pomegranate juice that protects cultured syncytiotrophoblasts from stress-induced apoptosis. Here, we test the hypothesis that punicalagin has this effect by inhibiting the mTOR kinase pathway to enhance autophagic turnover and limit apoptosis in cultured primary human syncytiotrophoblasts. In syncytiotrophoblasts, starvation, rapamycin, or punicalagin all decreased the expression of phosphorylated ribosomal protein S6, a downstream target of the mTOR kinase, and of the autophagy markers, LC3-II and p62. In contrast, in the presence of bafilomycin, an inhibitor of late stages of autophagy and degradation in the autophagolysosome, syncytiotrophoblasts exposed to starvation, rapamycin, or punicalagin all showed increased levels of LC3-II and p62. The number of LC3-II punctae also increased in punicalagin-treated syncytiotrophoblasts exposed to chloroquine, another inhibitor of autophagic degradation, and punicalagin increased the number of lysosomes. The apoptosis-reducing effect of punicalagin was attenuated by inhibition of autophagy using bafilomycin or knockdown of the autophagy related gene,ATG16L1. Collectively, these data support the hypothesis that punicalagin modulates the crosstalk between autophagy and apoptosis to promote survival in cultured syncytiotrophoblasts.

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Tuan, R. S., C. J. Moore, J. W. Brittingham, J. J. Kirwin, R. E. Akins, and M. Wong. "In vitro study of placental trophoblast calcium uptake using JEG-3 human choriocarcinoma cells." Journal of Cell Science 98, no. 3 (March 1, 1991): 333–42. http://dx.doi.org/10.1242/jcs.98.3.333.

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During human fetal development, placental syncytiotrophoblasts actively transport calcium from the maternal to the fetal circulation. Two functional components, a cytosolic Ca2(+)-binding protein (CaBP) and a Ca2(+)-ATPase have been identified in the syncytiotrophoblasts of the chorionic villi. We report here the calcium uptake properties of a human choriocarcinoma cell line, JEG-3, which was used as an in vitro model cell system for the syncytiotrophoblasts. In culture, JEG-3 proliferated as large syncytial aggregates expressing typical syncytiotrophoblast markers. 45Ca uptake by JEG-3 was a substrate- and temperature-dependent, membrane-mediated active process that exhibited linear kinetics for up to 7 min. Both the CaBP and the Ca2(+)-ATPase were expressed by JEG-3, on the basis of biochemical, histochemical, immunochemical and or mRNA assays. Immunohistochemistry and in situ hybridization revealed that JEG-3 cells were heterogeneous with respect to the expression of the CaBP. The Ca2(+)-ATPase activity of JEG-3 was similar to the placental enzyme in terms of sensitivity to specific inhibitors, and was detected histochemically along the cell membrane. Fura-2 Ca2+ imaging revealed that calcium uptake by JEG-3 was not accompanied by a concomitant increase in cytosolic [Ca2+], suggesting a specific Ca2+ sequestration mechanism. The involvement of calciotropic hormonal regulation was evaluated by studying the response of JEG-3 to 1,25-dihydroxy vitamin D3. Calcium uptake was significantly stimulated in a dose-dependent manner by a 24-h treatment of the cells with 1,25-dihydroxy vitamin D3 (optimal dose approximately 0.5 nM); the CaBP level doubled whereas steady-state CaBP mRNA did not, suggesting that CaBP expression was regulated by 1,25-dihydroxy vitamin D3. These observations strongly suggest that the JEG-3 human choriocarcinoma cells should serve as a convenient in vitro model system for studying the cellular mechanism and regulation of transplacental calcium transport.

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Duello, T. M., P. J. Bertics, D. L. Fulgham, and P. J. Van Ess. "Localization of epidermal growth factor receptors in first- and third-trimester human placentas." Journal of Histochemistry & Cytochemistry 42, no. 7 (July 1994): 907–15. http://dx.doi.org/10.1177/42.7.8014474.

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Studies to date have demonstrated epidermal growth factor (EGF) receptors primarily on the outer plasma membrane of the human placental syncytiotrophoblasts facing maternal blood and to a lesser extent on the cytotrophoblast stem cells. In the present studies, first- and third-trimester human placental tissues were immunostained with monoclonal antibodies (MAb) to the EGF binding domain of the human EGF receptor or to the activated (tyrosine-phosphorylated) human EGF receptor. Cytotrophoblasts, syncytiotrophoblasts, and fetal connective tissue cells in first-trimester tissues immunostained with both MAb, with the notable exception of the absence of staining of activated EGF receptor over cytotrophoblast plasma membranes. In contrast, staining of third-trimester placentas with either MAb yielded little to no staining of either trophoblast cell layer but intense staining of fetal connective tissue cells. Staining for EGF receptors over cytotrophoblasts in the first trimester is consistent with the hypothesis that maternal EGF or TGF-alpha derived from the endometrium or placenta may be the mitogen responsible for cytotrophoblast cell division and that the receptors localized to the syncytiotrophoblast are involved in EGF regulation of differentiated function. The absence of heavy staining of activated EGF receptor on trophoblast plasma membranes in third-trimester placentas is consistent with down-regulation of EGF receptor activity.

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Ceri, Howard, Wei Sek Hwang, and Helen Cheung. "Endogenous heparin-binding lectin activity in human placenta: purification and developmental expression." Biochemistry and Cell Biology 68, no. 4 (April 1, 1990): 790–95. http://dx.doi.org/10.1139/o90-113.

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Human placental extracts contain a herapin-inhibitable lectin activity. The lectin, which closely resembles those from chicken and rat tissues, was purified by heparin-affinity chromatography. It shares many properties with the previously reported lectins, including hapten specificity, molecular weight of monomers, and immunological cross-reactivity. Sections from different stages of placental development, stained by immunohistochemistry procedures using lectin-specific antibody, showed that the lectin was initially present only in cytotrophoblasts of early first trimester villi. Later in the first trimester, both cytotrophoblasts and syncytiotrophoblasts were stained positively for lectin. From second trimester to term, the lectin was seen only in syncytiotrophoblasts.Key words: lectin, human placenta, development, heparin, cytotrophoblast, syncytiotrophoblast.

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Pepe, Gerald J., Marcia G. Burch, Colin P. Sibley, William A. Davies, and Eugene D. Albrecht. "Expression of the mRNAs and Proteins for the Na+/H+ Exchangers and Their Regulatory Factors in Baboon and Human Placental Syncytiotrophoblast." Endocrinology 142, no. 8 (August 1, 2001): 3685–92. http://dx.doi.org/10.1210/endo.142.8.8343.

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Abstract In polarized epithelial cells of several organ systems, e.g. the kidney, a family of Na+/H+ exchangers (e.g. Na+/H+ exchanger-1 and -3) and their regulatory proteins, Na+/H+ exchanger regulatory factor and Na+/H+ exchanger-3 kinase A regulatory protein play a major role in regulating Na+/H+ exchange integral to cellular homeostasis. Because the primate placenta regulates exchange of Na+ and H+ between the mother and fetus critical to fetal-placental homeostasis, the current study determined whether Na+/H+ exchanger-1 and -3 were compartmentalized and associated with expression of Na+/H+ exchanger regulatory factor and Na+/H+ exchanger-3 kinase A regulatory protein in baboon and human syncytiotrophoblast. Using RT-PCR, single 413-bp Na+/H+ exchanger-1 and 190-bp Na+/H+ exchanger-3 products were expressed by baboon and human syncytiotrophoblasts. The 104-kDa Na+/H+ exchanger-1 protein was detected by Western blot in microvillus membranes and to a much lesser extent in the basal membranes of the baboon and human syncytiotrophoblasts. In contrast, the 85-kDa Na+/H+ exchanger-3 protein was detected primarily in membranes contiguous with the basal membranes of the syncytiotrophoblast of both species. Differential localization of Na+/H+ exchanger-1 and -3 was confirmed by immunocytochemistry. The Na+/H+ exchanger-3 regulatory protein, Na+/H+ exchanger-3 kinase A regulatory protein, resided almost exclusively in the basal membranes, whereas Na+/H+ exchanger regulatory factor was localized primarily to the microvillus membranes in the baboon and human syncytiotrophoblast. Collectively, these results are the first to show that the baboon and human term placental syncytiotrophoblast expressed the mRNAs and proteins for Na+/H+ exchanger-1 and -3 and their regulatory factors and that Na+/H+ exchanger-1 and Na+/H+ exchanger regulatory factor resided primarily in the microvillus membranes, whereas Na+/H+ exchanger-3 and Na+/H+ exchanger-3 kinase A regulatory protein were localized to membranes contiguous with the basal membranes and to the basal membranes, respectively. We conclude that a complete Na+/H+ exchange system is present in the baboon and human term placental syncytiotrophoblast and suggest that the primate placenta exhibits polarity with respect to the capacity for regulation of Na+/H+ exchange between the placenta and the maternal and fetal circulations.

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Tarrade, Anne, Kristina Schoonjans, Jean Guibourdenche, Jean Michel Bidart, Michel Vidaud, Johan Auwerx, Cécile Rochette-Egly, and Danièle Evain-Brion. "PPARγ/RXRα Heterodimers Are Involved in Human CGβ Synthesis and Human Trophoblast Differentiation." Endocrinology 142, no. 10 (October 1, 2001): 4504–14. http://dx.doi.org/10.1210/endo.142.10.8448.

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Abstract Recent studies performed with null mice suggested a role of either RXRα or PPARγ in murine placental development. We report here that both PPARγ and RXRα are strongly expressed in human villous cytotrophoblasts and syncytiotrophoblasts. Moreover, specific ligands for RXRs or PPARγ (but not for PPARα or PPARδ) increase both human CGβ transcript levels and the secretion of human CG and its free β-subunit. When combined, these ligands have an additive effect on human CG secretion. Pan-RXR and PPARγ ligands also have an additive effect on the synthesis of other syncytiotrophoblast hormones such as human placental lactogen, human placental GH, and leptin. Therefore, in human placenta, PPARγ/RXRα heterodimers are functional units during cytotrophoblast differentiation into the syncytiotrophoblast in vitro. Elements located in the regulatory region of the human CGβ gene (β5) were found to bind RXRα and PPARγ from human cytotrophoblast nuclear extracts, suggesting that PPARγ/RXRα heterodimers directly regulate human CGβ transcription. Altogether, these data show that PPARγ/RXRα heterodimers play an important role in human placental development.

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Fisher, Susan, Olga Genbacev, Ekaterina Maidji, and Lenore Pereira. "Human Cytomegalovirus Infection of Placental Cytotrophoblasts In Vitro and In Utero: Implications for Transmission and Pathogenesis." Journal of Virology 74, no. 15 (August 1, 2000): 6808–20. http://dx.doi.org/10.1128/jvi.74.15.6808-6820.2000.

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ABSTRACT Human cytomegalovirus (CMV) is the leading cause of prenatal viral infection. Affected infants may suffer intrauterine growth retardation and serious neurologic impairment. Analysis of spontaneously aborted conceptuses shows that CMV infects the placenta before the embryo or fetus. In the human hemochorial placenta, maternal blood directly contacts syncytiotrophoblasts that cover chorionic villi and cytotrophoblasts that invade uterine vessels, suggesting possible routes for CMV transmission. To test this hypothesis, we exposed first-trimester chorionic villi and isolated cytotrophoblasts to CMV in vitro. In chorionic villi, syncytiotrophoblasts did not become infected, although clusters of underlying cytotrophoblasts expressed viral proteins. In chorionic villi that were infected with CMV in utero, syncytiotrophoblasts were often spared, whereas cytotrophoblasts and other cells of the villous core expressed viral proteins. Isolated cytotrophoblasts were also permissive for CMV replication in vitro; significantly, infection subsequently impaired the cytotrophoblasts' ability to differentiate and invade. These results suggest two possible routes of CMV transmission to the fetus: (i) across syncytiotrophoblasts with subsequent infection of the underlying cytotrophoblasts and (ii) via invasive cytotrophoblasts within the uterine wall. Furthermore, the observation that CMV infection impairs critical aspects of cytotrophoblast function offers testable hypotheses for explaining the deleterious effects of this virus on pregnancy outcome.

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Ge, Y. C., J. N. Li, X. T. Ni, C. M. Guo, W. S. Wang, T. Duan, and K. Sun. "Cross talk between cAMP and p38 MAPK pathways in the induction of leptin by hCG in human placental syncytiotrophoblasts." REPRODUCTION 142, no. 2 (August 2011): 369–75. http://dx.doi.org/10.1530/rep-11-0053.

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Leptin produced by the placental syncytiotrophoblasts participates in a number of processes in pregnancy including implantation, proliferation of the cytotrophoblasts, and nutrient transfer across the placenta. Despite the functional significance of leptin in pregnancy, the regulation of leptin synthesis is poorly understood in human placental syncytiotrophoblasts. In this study, we investigated the role of endogenous human chorionic gonadotropin (hCG) in the regulation of leptin production as well as the underlying mechanism involving the cross talk between cAMP and p38 mitogen-activated protein kinase (MAPK) pathways. We found that neutralization of endogenous hCG with its antibody dose dependently decreased leptin mRNA level and secretion, whereas exogenous hCG increased leptin mRNA level and secretion. Activation of the cAMP pathway with dibutyryl cAMP (db cAMP) or forskolin recapitulated the stimulatory effect of hCG on leptin expression. Inhibition of protein kinase A with H89 not only reduced the basal leptin expression but also attenuated the induced leptin expression by hCG. Treatment of the syncytiotrophoblasts with db cAMP and hCG phosphorylated p38 MAPK. Inhibition of p38 MAPK with SB203580 not only reduced the basal leptin production but also attenuated the leptin-induced production by both hCG and db cAMP. These data suggest that endogenous hCG plays a significant role in maintaining leptin production in human placental syncytiotrophoblasts, and this effect involves a cross talk between cAMP and p38 MAPK pathways.

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Alison, R. H., D. J. Lewis, and C. A. Montgomery. "Ovarian Choriocarcinoma in the Mouse." Veterinary Pathology 24, no. 3 (May 1987): 226–30. http://dx.doi.org/10.1177/030098588702400305.

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Choriocarcinoma is one of the rarest ovarian tumors in any animal species. This paper describes the gross and microscopic appearance of seven such neoplasms in B6C3F1 mice. Mean age at death was 47 weeks. Tumors were described at necropsy as dark or hemorrhagic cystic lesions. On microscopic examination tumors were composed of hematocysts, intercellular hemorrhage, and cytotrophoblasts, syncytiotrophoblasts, and/or trophoblastic giant cells. Cytotrophoblasts, syncytiotrophoblasts, and occasional giant cells were present in three cases while the other four tumors contained only trophoblastic giant cells.

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Toyosawa, K., K. Okimoto, T. Koujitani, and E. Kikawa. "Choriocarcinoma and Teratoma in the Ovary of a Cynomolgus Monkey." Veterinary Pathology 37, no. 2 (March 2000): 186–88. http://dx.doi.org/10.1354/vp.37-2-186.

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An ovarian choriocarcinoma was found in a 13-year-old cynomolgus monkey ( Macaca fascicularis). The tumor was accompanied by a mature teratoma in the contralateral ovary. Histologically, the choriocarcinoma was characterized by nests of cells where cytotrophoblasts occupied the periphery with syncytiotrophoblasts at the center. Immunohistochemical staining for anti-human chorionic gonadotropin was positive in the syncytiotrophoblasts. The teratoma consisted of well-differentiated epidermal cells, sebaceous glands, hair follicles, cartilage, bone, and teeth. Choriocarcinoma metastases were in multiple organs. The concomitant development of choriocarcinoma and teratoma in the ovary is a consistent finding with the human counterparts of these lesions.

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Chamley, L., C. Viall, P. Stone, and Q. Chen. "528. THE INTERNALIZATION OF ANTIPHOSPHOLIPID ANTIBODIES INTO TROPHOBLASTS CORRELATES WITH THE EXPRESSION OF MEGALIN." Reproduction, Fertility and Development 21, no. 9 (2009): 127. http://dx.doi.org/10.1071/srb09abs528.

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Antiphospholipid antibodies (aPL) are autoantibodies that increase the risk of preeclampsia nine fold. We have recently shown aPL increase in the number of syncytial knots shed from placental explants and also change the trophoblast death process towards necrosis. Shedding of necrotic syncytial knots is thought to contribute to the pathogenesis of preeclampsia. Antiphospholipid antibodies but not control antibodies, are internalised into the syncytiotrophoblast suggesting a specific mechanism for internalisation of the aPL. Megalin is known to be an endocytic receptor for the antigen of aPL. We believe that the internalisation of aPL into the syncytiotrophoblast is required to for aPL to affect trophoblast shedding and in this study began to investigate the hypothesis that megalin mediates aPL-internalisation. Monoclonal aPL, IIC5 or ID2, were incubated with monolayers of the trophoblast cell lines, Jar, Jeg 3 or BeWo, or first trimester placental explants for 24 hours. Internalisation of aPL into trophoblasts was determined by fluorescent immuno-staining as was the expression of megalin using an antimegalin antibody (Sigma). Experiments were repeated at least three times. Confocal microscopy demonstrated that the syncytiotrophoblast of explants and BeWo cells, but not Jar or Jeg3 cells, internalised the aPL. Despite treating explants and BeWos with the same amount of aPL the level of aPL internalised by the syncytiotrophoblast of explants was greater than the level internalised by BeWos. Megalin was expressed strongly by the syncytiotrophoblast and weakly by BeWos but was not expressed by Jars or Jeg3 cells. The internalization of aPL into syncytiotrophoblasts may play an important role in regulating trophoblast death leading to aberrant shedding of syncytial knots. This study provides preliminary evidence that megalin expression correlates with the ability of trophoblasts to internalize aPL suggesting it may be the receptor that mediates aPL internalization into trophoblasts making this pathway a potential therapeutic target.

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Leitner, Karl, Roman Szlauer, Isabella Ellinger, Adolf Ellinger, Klaus-Peter Zimmer, and Renate Fuchs. "Placental Alkaline Phosphatase Expression at the Apical and Basal Plasma Membrane in Term Villous Trophoblasts." Journal of Histochemistry & Cytochemistry 49, no. 9 (September 2001): 1155–64. http://dx.doi.org/10.1177/002215540104900909.

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Human placental alkaline phosphatase (PLAP) was localized at the apical and basal plasma membrane of syncytiotrophoblasts and at the surface of cytotrophoblasts in term chorionic villi using immunoelectron microscopy. Similarly, apical and basolateral PLAP expression was found in polarized trophoblast-derived BeWo cells. Trophoblasts isolated from term placentas exhibited mainly vesicular PLAP immunofluorescence staining immediately after isolation. After in vitro differentiation into syncytia, PLAP plasma membrane expression was upregulated and exceeded that observed in mononuclear trophoblasts. These data call for caution in using PLAP as a morphological marker to differentiate syncytiotrophoblasts from cytotrophoblasts or as a marker enzyme for placental brush-border membranes. (J Histochem Cytochem 49:1155–1164, 2001)

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Broeder, J. A., C. H. Smith, and A. J. Moe. "Glutamate oxidation by trophoblasts in vitro." American Journal of Physiology-Cell Physiology 267, no. 1 (July 1, 1994): C189—C194. http://dx.doi.org/10.1152/ajpcell.1994.267.1.c189.

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Catabolism of uniformly and 1-14C-labeled glutamate was investigated in human placental cytotrophoblasts and syncytiotrophoblasts cultured on uncoated plastic or a fibrin matrix. Product-labeling experiments resulted in 14C incorporation into carbon dioxide and tricarboxylic acid cycle intermediates. 14C incorporation above background was not detected for the putative products, glutamine, amino acids, glutathione, and protein. Inhibitors of specific metabolic pathways were used to elucidate the routes of glutamate oxidation. Incorporation of 14C into carbon dioxide from [1-14C]glutamate was inhibited by the glutamate dehydrogenase inhibitor pyridine-2,6-dicarboxylic acid and aminotransferase inhibitor aminooxyacetic acid. Production of 14CO2 was higher for syncytiotrophoblast compared with cytotrophoblast and for cells on uncoated plastic compared with a fibrin matrix. Oxidation of glutamate was unaffected by added glutamine as high as 2 mM. The primary route of glutamate metabolism by placental trophoblast in vitro is oxidation to carbon dioxide utilizing both the transferase and deamination pathways.

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Corry, Jacqueline, Nitin Arora, Charles A. Good, Yoel Sadovsky, and Carolyn B. Coyne. "Organotypic models of type III interferon-mediated protection from Zika virus infections at the maternal–fetal interface." Proceedings of the National Academy of Sciences 114, no. 35 (August 7, 2017): 9433–38. http://dx.doi.org/10.1073/pnas.1707513114.

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Protecting the fetus from the hematogenous spread of viruses requires multifaceted layers of protection and relies heavily on trophoblasts, the fetal-derived cells that comprise the placental barrier. We showed previously that trophoblasts isolated from full-term placentas resist infection by diverse viruses, including Zika virus (ZIKV), and transfer this resistance to nonplacental cells through the activity of paracrine effectors, including the constitutive release of type III interferons (IFNs). Here, we developed 3D cell-line–based models of human syncytiotrophoblasts, cells that lie in direct contact with maternal blood, and show that these cells recapitulate the antiviral properties of primary trophoblasts through the constitutive release of type III IFNs (IFNλ1 and IFNλ2) and become resistant to ZIKV infection. In addition, using organotypic human midgestation chorionic villous explants, we show that syncytiotrophoblasts isolated from the second trimester of pregnancy also constitutively release type III IFNs and use these IFNs in autocrine and paracrine manners to restrict ZIKV infection. Collectively, these data provide important insights into the defense mechanisms used by syncytiotrophoblasts at various stages of human gestation to resist ZIKV infection and new human models to study the role of type III IFNs in the vertical transmission of ZIKV and other viruses associated with congenital disease.

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Chen, Baosheng, Mark S. Longtine, and D. Michael Nelson. "Punicalagin, a polyphenol in pomegranate juice, downregulates p53 and attenuates hypoxia-induced apoptosis in cultured human placental syncytiotrophoblasts." American Journal of Physiology-Endocrinology and Metabolism 305, no. 10 (November 15, 2013): E1274—E1280. http://dx.doi.org/10.1152/ajpendo.00218.2013.

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Oxidative stress is associated with placental dysfunction and suboptimal pregnancy outcomes. Therapeutic interventions to limit placental injury from oxidative stress are lacking. Punicalagin is an ellagitannin and a potent antioxidant in pomegranate juice. We showed that both pomegranate juice and punicalagin decrease oxidative stress and apoptosis in cultured syncytiotrophoblasts. p53 is involved in the oxidative stress-induced apoptosis in trophoblasts. We now test the hypothesis that punicalagin limits trophoblast injury in vitro by regulating the levels of p53. We examined the expression of p53, mouse double minute 2 homolog, p21, hypoxia-inducible factor (HIF) α, and selected members of the B cell lymphoma 2 (BCL2) family of proteins in cultured syncytiotrophoblasts exposed to ≤1% oxygen in the absence or presence of punicalagin. We found that punicalagin attenuated hypoxia-induced apoptosis in syncytiotrophoblasts, as quantified by levels of cleaved poly-ADP ribose polymerase. This protective effect was in part mediated by reduced p53 activity shown by decreased expression of p21, lower HIF1α expression, and limited activity of caspases 9 and 3. There was no change in expression of proteins in the BCL2 family, which are also important in apoptosis. The data support a role for downregulation of p53 in the protection of human trophoblasts by punicalagin.

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Storm, Tina, Erik I. Christensen, Julie Nelly Christensen, Tine Kjaergaard, Niels Uldbjerg, Agnete Larsen, Bent Honoré, and Mette Madsen. "Megalin Is Predominantly Observed in Vesicular Structures in First and Third Trimester Cytotrophoblasts of the Human Placenta." Journal of Histochemistry & Cytochemistry 64, no. 12 (October 23, 2016): 769–84. http://dx.doi.org/10.1369/0022155416672210.

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The membrane receptor megalin is crucial for normal fetal development. Besides its expression in the developing fetus, megalin is also expressed in the human placenta. Similar to its established function in the kidney proximal tubules, placental megalin has been proposed to mediate uptake of vital nutrients. However, details of megalin expression, subcellular localization, and function in the human placenta remain to be established. By immunohistochemical analyses of first trimester and term human placenta, we showed that megalin is predominantly expressed in cytotrophoblasts, the highly proliferative cells in placenta. Only limited amounts of megalin could be detected in syncytiotrophoblasts and least in term placenta syncytiotrophoblasts. Immunocytochemical analyses furthermore showed that placental megalin associates with structures of the endolysosomal apparatus. Combined, our results clearly place placental megalin in the context of endocytosis and trafficking of ligands. However, due to the limited expression of megalin in syncytiotrophoblasts, especially in term placenta, it appears that the main role for placental megalin is not to mediate uptake of nutrients from the maternal bloodstream, as previously proposed. In contrast, our results point toward novel and complex functions for megalin in the cytotrophoblasts. Thus, we propose that the perception of placental megalin localization and function should be revised.

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Masoumi, Zahra, Lena Erlandsson, Eva Hansson, Mattias Magnusson, Eva Mezey, and Stefan R. Hansson. "Hypoxia-Induced Alpha-Globin Expression in Syncytiotrophoblasts Mimics the Pattern Observed in Preeclamptic Placentas." International Journal of Molecular Sciences 22, no. 7 (March 25, 2021): 3357. http://dx.doi.org/10.3390/ijms22073357.

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Preeclampsia (PE) is a pregnancy disorder associated with placental dysfunction and elevated fetal hemoglobin (HbF). Early in pregnancy the placenta harbors hematopoietic stem and progenitor cells (HSPCs) and is an extramedullary source of erythropoiesis. However, globin expression is not unique to erythroid cells and can be triggered by hypoxia. To investigate the role of the placenta in increasing globin levels previously reported in PE, flow cytometry, histological and immunostaining and in situ analyses were used on placenta samples and ex vivo explant cultures. Our results indicated that in PE pregnancies, placental HSPC homing and erythropoiesis were not affected. Non-erythroid alpha-globin mRNA and protein, but not gamma-globin, were detected in syncytiotrophoblasts and stroma of PE placenta samples. Similarly, alpha-globin protein and mRNA were upregulated in normal placenta explants cultured in hypoxia. The upregulation was independent of HIF1 and NRF2, the two main candidates of globin transcription in non-erythroid cells. Our study is the first to demonstrate alpha-globin mRNA expression in syncytiotrophoblasts in PE, induced by hypoxia. However, gamma-globin was only expressed in erythrocytes. We conclude that alpha-globin, but not HbF, is expressed in placental syncytiotrophoblasts in PE and may contribute to the pathology of the disease.

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Tomi, Masatoshi, Hiromi Eguchi, Mayuko Ozaki, Tomohiro Tawara, Sachika Nishimura, Kei Higuchi, Tetsuo Maruyama, Tomohiro Nishimura, and Emi Nakashima. "Role of OAT4 in Uptake of Estriol Precursor 16α-Hydroxydehydroepiandrosterone Sulfate Into Human Placental Syncytiotrophoblasts From Fetus." Endocrinology 156, no. 7 (April 28, 2015): 2704–12. http://dx.doi.org/10.1210/en.2015-1130.

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Estriol biosynthesis in human placenta requires the uptake of a fetal liver-derived estriol precursor, 16α-hydroxydehydroepiandrosterone sulfate (16α-OH DHEAS), by placental syncytiotrophoblasts at their basal plasma membrane (BM), which faces the fetal circulation. The aim of this work is to identify the transporter(s) mediating 16α-OH DHEAS uptake at the fetal side of syncytiotrophoblasts by using human placental BM-enriched vesicles and to examine the contribution of the putative transporter to estriol synthesis at the cellular level, using choriocarcinoma JEG-3 cells. Organic anion transporter (OAT)-4 and organic anion transporting polypeptide 2B1 proteins were enriched in human placental BM vesicles compared with crude membrane fraction. Uptake of [3H]16α-OH DHEAS by BM vesicles was partially inhibited in the absence of sodium but was significantly increased in the absence of chloride and after preloading glutarate. Uptake of [3H]16α-OH DHEAS by BM vesicles was significantly inhibited by OAT4 substrates such as dehydroepiandrosterone sulfate, estrone-3-sulfate, and bromosulfophthalein but not by cyclosporin A, tetraethylammonium, p-aminohippuric acid, or cimetidine. These characteristics of vesicular [3H]16α-OH DHEAS uptake are in good agreement with those of human OAT4-transfected COS-7 cells as well as forskolin-differentiated JEG-3 cells. Estriol secretion from differentiated JEG-3 cells was detected when the cells were incubated with 16α-OH DHEAS for 8 hours but was inhibited in the presence of 50 μM bromosulfophthalein. Our results indicate that OAT4 at the BM of human placental syncytiotrophoblasts plays a predominant role in the uptake of 16α-OH DHEAS for placental estriol synthesis.

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Nadeau, Valérie, and Jean Charron. "Importance of the ERK/MAPK pathway in syncytiotrophoblasts differentiation." Developmental Biology 331, no. 2 (July 2009): 479–80. http://dx.doi.org/10.1016/j.ydbio.2009.05.350.

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Barrera, David, Euclides Avila, Guillermo Hernandez, Isabel Mendez, Leticia Gonzalez, Ali Halhali, Fernando Larrea, Angelica Morales, and Lorenza Diaz. "Calcitriol affects hCG gene transcription in cultured human syncytiotrophoblasts." Reproductive Biology and Endocrinology 6, no. 1 (2008): 3. http://dx.doi.org/10.1186/1477-7827-6-3.

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Shimono, Aiko, Yuko Imoto, Haruhiko Sakamoto, Yoichi Chiba, Koichi Matsumoto, Machi Kawauchi, Takashi Kusaka, et al. "An immunohistochemical study of placental syncytiotrophoblasts in neonatal hemochromatosis." Placenta 48 (December 2016): 49–55. http://dx.doi.org/10.1016/j.placenta.2016.10.005.

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Prince, Calais, Alina Maloyan, and Leslie Myatt. "Manipulation of TRKB activation alters cellular respiration in syncytiotrophoblasts." Placenta 45 (September 2016): 66–67. http://dx.doi.org/10.1016/j.placenta.2016.06.023.

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Lee, Lydia, Fernanda Heitor, Harvey Kliman, Thomas Mcelrath, and Joseph Majzoub. "Syncytiotrophoblasts of preeclamptic placentas overexpress corticotropin-releasing hormone mRNA." American Journal of Obstetrics and Gynecology 195, no. 6 (December 2006): S18. http://dx.doi.org/10.1016/j.ajog.2006.10.048.

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Nedder, Margaux, Sonja Boland, Stéphanie Devineau, Amal Zerrad-Saadi, Jasmina Rogozarski, René Lai-Kuen, Ibtissem Baya, et al. "Uptake of Cerium Dioxide Nanoparticles and Impact on Viability, Differentiation and Functions of Primary Trophoblast Cells from Human Placenta." Nanomaterials 10, no. 7 (July 3, 2020): 1309. http://dx.doi.org/10.3390/nano10071309.

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The human placenta is at the interface between maternal and fetal circulations, and is crucial for fetal development. The nanoparticles of cerium dioxide (CeO2 NPs) from air pollution are an unevaluated risk during pregnancy. Assessing the consequences of placenta exposure to CeO2 NPs could contribute to a better understanding of NPs’ effect on the development and functions of the placenta and pregnancy outcome. We used primary villous cytotrophoblasts purified from term human placenta, with a wide range of CeO2 NPs concentrations (0.1–101 μg/cm2) and exposure time (24–72 h), to assess trophoblast uptake, toxicity and impact on trophoblast differentiation and endocrine function. We have shown the capacity of both cytotrophoblasts and syncytiotrophoblasts to internalize CeO2 NPs. CeO2 NPs affected trophoblast metabolic activity in a dose and time dependency, induced caspase activation and a LDH release in the absence of oxidative stress. CeO2 NPs decreased the fusion capacity of cytotrophoblasts to form a syncytiotrophoblast and disturbed secretion of the pregnancy hormones hCG, hPL, PlGF, P4 and E2, in accordance with NPs concentration. This is the first study on the impact of CeO2 NPs using human primary trophoblasts that decrypts their toxicity and impact on placental formation and functions.

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Omigbodun, Akinyinka, Piotr Ziolkiewicz, Cheryl Tessler, John R. Hoyer, and Christos Coutifaris. "Progesterone Regulates Osteopontin Expression in Human Trophoblasts: A Model of Paracrine Control in the Placenta?*." Endocrinology 138, no. 10 (October 1, 1997): 4308–15. http://dx.doi.org/10.1210/endo.138.10.5431.

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Abstract Osteopontin (OPN), a matrix glycosylated phosphoprotein, has been proposed to play a role(s) in basic cellular processes, such as neovascularization and tissue remodeling, which are essential to placental morphogenesis and embryo implantation. We have shown OPN to be expressed by cytotrophoblasts of the chorionic villus, and a putative progesterone regulatory element in the OPN promoter suggests hormonal regulatory control. This led us to test the hypothesis that progesterone regulates OPN expression in human cytotrophoblasts. Cytotrophoblasts isolated from human placentas were treated with combinations of progesterone, RU486, and/or aminoglutethimide, and their expression of OPN was assessed by Northern hybridization and immunocytochemistry. The expression of OPN messenger RNA (mRNA) declined as trophoblasts aggregated, but rebounded at later times when syncytia and mononuclear cytotrophoblasts coexisted in culture. Progesterone increased OPN mRNA expression by aggregating mononuclear cytotrophoblasts. Aminoglutethimide suppression of endogenous steroidogenesis by syncytiotrophoblasts inhibited OPN expression, whereas the addition of exogenous progesterone to cells treated with aminoglutethimide reversed this inhibitory effect. These observations were confirmed at the protein level by immunocytochemistry. Treatment of cytotrophoblasts with both progesterone and RU486 inhibited the up-regulatory effect on OPN mRNA associated with exposure to progesterone alone, further confirming a direct effect of progesterone. We conclude that progesterone up-regulates OPN expression in human cytotrophoblasts, and we propose that in vivo, progesterone secretion by syncytiotrophoblasts regulates the expression of OPN by the underlying cytotrophoblasts. As the receptors for OPN,α v integrins, are expressed by syncytiotrophoblasts, we postulate that these paracrine regulatory mechanisms contribute to the adhesive and/or signaling events between the two trophoblast cell types of the chorionic villus.

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Austgulen, Rigmor, Lisa Chedwick, Christina Vogt Isaksen, Lars Vatten, and Catherine Craven. "Trophoblast Apoptosis in Human Placenta at Term as Detected by Expression of a Cytokeratin 18 Degradation Product of Caspase." Archives of Pathology & Laboratory Medicine 126, no. 12 (December 1, 2002): 1480–86. http://dx.doi.org/10.5858/2002-126-1480-taihpa.

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Abstract Context.—Apoptosis occurs in the normal placenta. The monoclonal antibody M30 is directed against a novel epitope of cytokeratin 18 (CK18) that is formed by caspase cleavage early in the apoptotic cascade, and this antibody may therefore be useful for evaluating trophoblast apoptosis. Objective.—We undertook the present study to evaluate the use of monoclonal antibody M30 to assess trophoblast apoptosis in placenta at term. Methods.—We stained paraffin-embedded placental tissues from 15 deliveries at term with M30. We compared positive M30 staining and CK18 staining (as detected by a monoclonal antibody directed against CK18) of trophoblasts in serial slides. We also compared apoptotic rates as detected by M30 and TUNEL (terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick end labeling) in 7 of the placentas. Results.—In fields of villous tissue, most M30-positive cells were CK18-positive syncytiotrophoblasts. Approximately half of M30-positive cells occurred as focal positive staining in the syncytial layer, and half occurred as abundant staining of syncytiotrophoblasts in areas with increased intervillous or perivillous fibrinoid. We found very few M30-positive cells in villous stroma. In decidual/basal plate tissues, most (two thirds) of the M30-positive cells were CK18-positive extravillous trophoblasts, whereas one third were syncytiotrophoblasts of anchoring villi. Since TUNEL detects apoptosis in both epithelial and nonepithelial cells, more cells were positively stained with TUNEL than with M30 in some tissue fields. However, our observations suggest that M30 was more sensitive than TUNEL in recognizing apoptotic trophoblasts and had less nonspecific staining than TUNEL. Conclusion.—We recommend the use of monoclonal antibody M30 for apoptosis studies in placental tissues. This antibody is easy to handle, the staining obtained seems specific, and the nonspecific staining seems negligible.

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STEFANER, Isabella, Anca STEFANESCU, Walter HUNZIKER, and Renate FUCHS. "Expression of placental alkaline phosphatase does not correlate with IgG binding, internalization and transcytosis." Biochemical Journal 327, no. 2 (October 15, 1997): 585–92. http://dx.doi.org/10.1042/bj3270585.

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The human homologue of FcRn, an IgG Fc receptor expressed in rat villous syncytiotrophoblasts, might be involved in IgG transfer from the maternal to the fetal circulation. However, because the receptor does not bind IgG at the physiological pH of the maternal blood (pH 7.4), FcRn is probably not involved in the initial uptake of IgG. A role in IgG internalization has been suggested for placental alkaline phosphatase (PLAP), which is highly expressed on the apical surface of syncytiotrophoblasts. To determine whether PLAP does indeed have a role in IgG uptake, we analysed the ability of PLAP to bind, internalize and transcytose IgG in BeWo choriocarcinoma cells endogenously expressing the protein, or in Madin-Darby canine kidney (MDCK) cells transfected with the PLAP cDNA. Although PLAP expression in MDCK cells resulted in increased IgG binding to intact cells, binding was not correlated with the level of PLAP expressed in the different cell lines. Furthermore our findings do not support a role for PLAP in IgG endocytosis or transcytosis.

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GOTO, SHIGENORI, KOICHI TAKAKUWA, KOJI KANAZAWA, and SHOSHICHI TAKEUCHI. "MLR-Blocking Antibodies Are Directed Against Alloantigens Expressed on Syncytiotrophoblasts." American Journal of Reproductive Immunology 21, no. 2 (October 1989): 50–53. http://dx.doi.org/10.1111/j.1600-0897.1989.tb01000.x.

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HEIKINHEIMO, M., O. SAKSELA, P. LEHTOVIRTA, M. SEPPÄLÄ, and H. BOHN. "CULTURED HUMAN SYNCYTIOTROPHOBLASTS SYNTHESIZE PREGNANCY-SPECIFIC BETA-1-GLYCOPROTEIN (SP1)." Acta Pathologica Microbiologica Scandinavica Section C Immunology 89C, no. 1-6 (August 15, 2009): 139–44. http://dx.doi.org/10.1111/j.1699-0463.1981.tb02677.x.

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Meng, Qian, Li Shao, Xiucui Luo, Yingping Mu, Wen Xu, Chao Gao, Li Gao, Jiayin Liu, and Yugui Cui. "Ultrastructure of Placenta of Gravidas with Gestational Diabetes Mellitus." Obstetrics and Gynecology International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/283124.

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Objectives. Gestational diabetes mellitus (GDM) leads to an abnormal placental environment which may cause some structural alterations of placenta and affect placental development and function. In this study, the ultrastructural appearances of term placentas from women with GDM and normal pregnancy were meticulously compared.Materials and Methods. The placenta tissues of term birth from 10 women with GDM and 10 women with normal pregnancy were applied with the signed informed consent. The morphology of fetomaternal interface of placenta was examined using light microscopy (LM) and transmission electron microscopy (TEM).Results. On LM, the following morphological changes in villous tissues were found in the GDM placentas when compared with the control placentas: edematous stroma, apparent increase in the number of syncytial knots, and perivillous fibrin deposition. On TEM, the distinct ultrastructural alterations indicating the degeneration of terminal villi were found in the GDM placentas as follows: thickening of the basal membrane (BM) of vasculosyncytial membrane (VSM) and the VSM itself, significantly fewer or even absent syncytiotrophoblastic microvilli, swollen or completely destroyed mitochondria and endoplasmic reticulum, and syncytiotrophoblasts with multiple vacuoles.Conclusion. Ultrastructural differences exist between GDM and control placentas. The differences of placenta ultrastructure are likely responsible for the impairment of placental barrier and function in GDM.

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Masuda, Junko, Eiji Takayama, Ayano Satoh, Michiru Ida, Tadashi Shinohara, Kyoko Kojima-Aikawa, Fumitaka Ohsuzu, et al. "Levels of annexin IV and V in the plasma of pregnant and postpartum women." Thrombosis and Haemostasis 91, no. 06 (2004): 1129–36. http://dx.doi.org/10.1160/th03-12-0778.

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SummaryAnnexin (Anx) V is pivotal in the maintenance of pregnancy by preventing the activation of blood coagulation. The homology of the amino acid sequence between Anx IV and Anx V is highest in Anx family proteins. However, little is known about the roles of Anx IV in pregnancy.The aim of this study is to clarify the roles of circulating Anx IV and Anx V in normal pregnancy. Subjects were non-pregnant women (n = 50), 120 pregnant women, and maternal subjects just after delivery (n = 53) or postpartum (n = 67). Anx IV in the plasma of non-pregnant women was at a concentration 20 times that of Anx V. The plasma levels of Anx IV suddenly increase after delivery, but Anx V levels remain low during this period. Anx IV and Anx V exert similar levels of anticoagulant activity. Anx IV protein was expressed on the basal surface of syncytiotrophoblasts; Anx V protein, on the apical surface of syncytiotrophoblasts. These results suggest that Anx IV enters the maternal bloodstream just after delivery and might play a role in preventing disseminated intravascular coagulopathy, and that Anx V helps to prevent clotting in the placenta during pregnancy.

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Frendo, Jean-Louis, Delphine Olivier, Valérie Cheynet, Jean-Luc Blond, Olivier Bouton, Michel Vidaud, Michèle Rabreau, Danièle Evain-Brion, and François Mallet. "Direct Involvement of HERV-W Env Glycoprotein in Human Trophoblast Cell Fusion and Differentiation." Molecular and Cellular Biology 23, no. 10 (May 15, 2003): 3566–74. http://dx.doi.org/10.1128/mcb.23.10.3566-3574.2003.

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ABSTRACT We recently demonstrated that the product of the HERV-W env gene, a retroviral envelope protein also dubbed syncytin, is a highly fusogenic membrane glycoprotein inducing the formation of syncytia on interaction with the type D mammalian retrovirus receptor. In addition, the detection of HERV-W Env protein (Env-W) expression in placental tissue sections led us to propose a role for this fusogenic glycoprotein in placenta formation. To evaluate this hypothesis, we analyzed the involvement of Env-W in the differentiation of primary cultures of human villous cytotrophoblasts that spontaneously differentiate by cell fusion into syncytiotrophoblasts in vitro. First, we observed that HERV-W env mRNA and glycoprotein expression are colinear with primary cytotrophoblast differentiation and with expression of human chorionic gonadotropin (hCG), a marker of syncytiotrophoblast formation. Second, we observed that in vitro stimulation of trophoblast cell fusion and differentiation by cyclic AMP is also associated with a concomitant increase in HERV-W env and hCG mRNA and protein expression. Finally, by using specific antisense oligonucleotides, we demonstrated that inhibition of Env-W protein expression leads to a decrease of trophoblast fusion and differentiation, with the secretion of hCG in culture medium of antisense oligonucleotide-treated cells being decreased by fivefold. Taken together, these results strongly support a direct role for Env-W in human trophoblast cell fusion and differentiation.

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Guilbert, L. J., M. Riddell, and B. Winkler-Lowen. "Caspase activation is not required for villous cytotrophoblast fusion into syncytiotrophoblasts." Placenta 31, no. 11 (November 2010): 982–88. http://dx.doi.org/10.1016/j.placenta.2010.08.012.

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Kovács, I. J., K. Hegedűs, A. Pál, and R. Pusztai. "Production of Proinflammatory Cytokines by Syncytiotrophoblasts Infected with Human Cytomegalovirus Isolates." Placenta 28, no. 7 (July 2007): 620–23. http://dx.doi.org/10.1016/j.placenta.2006.09.008.

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Ireland, Kayla E., Alina Maloyan, and Leslie Myatt. "Melatonin Improves Mitochondrial Respiration in Syncytiotrophoblasts From Placentas of Obese Women." Reproductive Sciences 25, no. 1 (April 26, 2017): 120–30. http://dx.doi.org/10.1177/1933719117704908.

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AL-OKAIL, MAJID S., and OMAR S. AL-ATTAS. "Histological Changes in Placental Syncytiotrophoblasts of Poorly Controlled Gestational Diabetic Patients." Endocrine Journal 41, no. 4 (1994): 355–60. http://dx.doi.org/10.1507/endocrj.41.355.

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Valent, Amy, Kevin Kolahi, and Kent Thornburg. "Glycolytic utilization and capacity of human cytotrophoblasts are higher than syncytiotrophoblasts." Placenta 45 (September 2016): 65–66. http://dx.doi.org/10.1016/j.placenta.2016.06.020.

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Marini, Camilla, Benjamin P. Lüscher, Daniel V. Surbek, and Marc U. Baumann. "GLUT1-down-regulation leads to a “premature senescence” in preeclamptic syncytiotrophoblasts." Placenta 45 (September 2016): 123–24. http://dx.doi.org/10.1016/j.placenta.2016.06.216.

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Golos, Thaddeus G., Lisa A. Krugner-Higby, Carolyn Stone Williams, Jennifer M. Fisher, Kimberly J. Johnson, Maureen Durning, and Kevin T. Schultz. "Primary cultures of rhesus placental syncytiotrophoblasts are permissive for SIV infection." Journal of Medical Primatology 23, no. 2-3 (February 5, 1994): 66–74. http://dx.doi.org/10.1111/j.1600-0684.1994.tb00104.x.

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Kristoffersen, Einar K., and Roald Matre. "Co-localization of β2-microglobulin and IgG in human placental syncytiotrophoblasts." European Journal of Immunology 26, no. 2 (February 1996): 505–7. http://dx.doi.org/10.1002/eji.1830260234.

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Brunette, M. G., and M. Leclerc. "Ca2+ transport through the brush border membrane of human placenta syncytiotrophoblasts." Canadian Journal of Physiology and Pharmacology 70, no. 6 (June 1, 1992): 835–42. http://dx.doi.org/10.1139/y92-112.

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The calcium (Ca2+) uptake by brush border membrane vesicles isolated from fresh human placentas has been characterized. This process was saturable and time- and concentration-dependent. It exhibited a double Michaelis–Menten kinetics, with apparent Km values of 0.17 ± 0.03 and 2.98 ± 0.17 mM Ca2+, and Vmax values of 0.9 ± 0.13 and 2.51 ± 0.45 pmol∙μg−1∙5 s−1. It was not influenced by the presence of Na+ or Mg2+ in the incubation medium. It was not increased by K+ or anion diffusion potentials, inside negative. At a steady state of 1 mM Ca2+ uptake, a large proportion (approximately 94%) of the Ca2+ was bound to the internal surface of the membranes. Preincubation of these membrane vesicles with voltage-dependent Ca2+ channel blockers (nifedipine and verapamil) had no influence on Ca2+ uptake. However, this uptake was very sensitive to pH. In the absence of a pH gradient, the Ca2+ uptake increased with alkalinity. When the intravesicular pH was kept constant while the pH of the incubation medium was increased, Ca2+ uptake was also stimulated by alkaline pH. In contrast, when the pH of the incubation medium was kept constant and the intravesicular pH was progressively increased, Ca2+ uptake was diminished with alkaline pH. Therefore, H+ gradient (H+ in trans-position > H+ in cis-position) favored Ca2+ transport, suggesting a H+/Ca2+ exchange mechanism. Finally, in contrast to the basal plasma membrane, the brash border membrane did not show any ATP-dependent Ca2+ transport activity.Key words: calcium transport, brush border membranes, placenta.

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Nelson, D. M., S. D. Smith, T. C. Furesz, Y. Sadovsky, V. Ganapathy, C. A. Parvin, and C. H. Smith. "Hypoxia reduces expression and function of system A amino acid transporters in cultured term human trophoblasts." American Journal of Physiology-Cell Physiology 284, no. 2 (February 1, 2003): C310—C315. http://dx.doi.org/10.1152/ajpcell.00253.2002.

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We tested the hypothesis that hypoxia diminishes the expression and transport of neutral amino acids by system A in full-term human trophoblasts. Cytotrophoblasts from normal human placentas were cultured in standard conditions of 20% O2 or in 1% and 3% O2 for 24 h before assay. Neutral amino acid transport for systems A, ASC, and L was assayed at 24 and 72 h by the cluster-tray technique. Hypoxia during the initial 24 h of culture reduced system A transport by 82% in 1% O2 and by 37% in 3% O2 ( P < 0.01) compared with standard conditions. Hypoxia during the latter 24 h of the 72 h in culture reduced system A transport by 55% in 1% O2 and by 20% in 3% O2 ( P < 0.05) compared with standard conditions at 72 h. Hypoxia (1% O2) also reduced total amino acid transport by 40% in the more differentiated syncytiotrophoblasts present at 72 h. Northern analysis of trophoblasts in standard conditions showed that subtypes of human amino acid transporter A (hATA1 and hATA2) were each expressed in cytotrophoblasts and syncytiotrophoblasts. Hypoxia decreased expression of hATA1 and hATA2 in both trophoblast phenotypes. We conclude that hypoxia downregulates system A transporter expression and activity in cultured human trophoblasts.

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Maidji, Ekaterina, Olga Genbacev, Hsin-Ti Chang, and Lenore Pereira. "Developmental Regulation of Human Cytomegalovirus Receptors in Cytotrophoblasts Correlates with Distinct Replication Sites in the Placenta." Journal of Virology 81, no. 9 (February 21, 2007): 4701–12. http://dx.doi.org/10.1128/jvi.02748-06.

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ABSTRACT Cytomegalovirus (CMV), the major viral cause of congenital disease, infects the uterus and developing placenta and spreads to the fetus throughout gestation. Virus replicates in invasive cytotrophoblasts in the decidua, and maternal immunoglobulin G (IgG)-CMV virion complexes, which are transcytosed by the neonatal Fc receptor across syncytiotrophoblasts, infect underlying cytotrophoblasts in chorionic villi. Immunity is central to protection of the placenta-fetal unit: infection can occur when IgG has a low neutralizing titer. Here we used immunohistochemical and function-blocking methods to correlate infection in the placenta with expression of potential CMV receptors in situ and in vitro. In placental villi, syncytiotrophoblasts express the virion receptor epidermal growth factor receptor (EGFR) but lack integrin coreceptors, and virion uptake occurs without replication. Focal infection can occur when transcytosed virions reach EGFR-expressing cytotrophoblasts that selectively initiate expression of αV integrin. In cell columns, proximal cytotrophoblasts lack receptors and distal cells express integrins α1β1 and αVβ3, enabling virion attachment. In the decidua, invasive cytotrophoblasts expressing coreceptors upregulate EGFR, thereby dramatically increasing susceptibility to infection. Our findings indicate that virion interactions with cytotrophoblasts expressing receptors in the placenta (i) change as the cells differentiate and (ii) correlate with spatially distinct sites of CMV replication in maternal and fetal compartments.

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Journal articles on the topic 'Syncytiotrophoblasts'

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