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- W3177125630 abstract "Vol. 129, No. 6 Science SelectionOpen AccessBPS and Cell Fusion in the Human Placenta: A Separate Mechanism of Action?is accompanied byBisphenol S and Epidermal Growth Factor Receptor Signaling in Human Placental Cytotrophoblasts Silke Schmidt Silke Schmidt Search for more papers by this author Published:29 June 2021CID: 064003https://doi.org/10.1289/EHP9248Cited by:1AboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit AbstractDuring the past decade, the plasticizer bisphenol S (BPS) has been replacing the endocrine-disrupting chemical bisphenol A (BPA) in numerous consumer products.1,2 As an example of its prevalence, a survey conducted in the United States and seven Asian countries found BPS in 81% of human urine samples collected.3 Despite the two chemicals’ general similarity, some of their biochemical properties differ.4,5,6 This raises the possibility that BPS may affect endocrine organs—including the human placenta—differently than BPA does. Researchers led by Almudena Veiga-Lopez, a visiting associate professor in the Department of Pathology at the University of Illinois at Chicago, explored one such mechanism in a recent in vitro study published in Environmental Health Perspectives.7BPS is used in thermal receipt paper and linings of food and beverage cans. It has been found in canned foods, indoor dust, sewage sludge, groundwater, and river sediment. Image: © Robert Hoetink/Shutterstock.Veiga-Lopez and colleagues studied cell fusion processes human placentas collected at the end of healthy pregnancies. The results of their analyses suggest that BPS may interfere with the formation of the syncytiotrophoblast (STB), a layer of epithelial cells in the placenta. The STB prevents the rejection of fetal cells by the maternal immune system, enables the exchange of nutrients and gases between mother and fetus, protects the fetus from some (although not all) harmful chemicals in maternal blood, and secretes its own hormones, such as hCG and progesterone.8The STB is composed of trophoblasts, which are the first cells to differentiate after an egg is fertilized. The authors proposed that BPS interferes with the fusion of trophoblasts into the STB by competing with the epidermal growth factor (EGF) for binding to the EGF receptor (EGFR). EGF is a protein that stimulates cell growth and differentiation throughout the body.9 The researchers analyzed trophoblasts from six term placentas and found that 200 nanograms per milliliter200 ng/mL of BPS blocked EGF-mediated cell fusion in vitro by binding to EGFR. That concentration is at the upper end of the reported urinary range for the U.S. general population.10Importantly, spontaneous cell fusion was not blocked by this dose, suggesting alternative mechanisms may be involved in the interference with STB formation. “Even if BPS were to block all of the cell fusion events that are induced by EGF, cells that were to fuse spontaneously—not through EGF—could still do so,” Veiga-Lopez explains.Although human trophoblasts from term placentas still fuse in vitro, they no longer divide.11,12 So the researchers also analyzed proliferating breast cancer cells, which are an established model for testing the EGFR-binding activity of environmental chemicals. The results provided additional evidence that BPS acts as an EGFR antagonist.The study raises the possibility that BPS may adversely affect fetal development or increase the risk of pregnancy complications. However, those possibilities hinge on the role of EGF in the cell fusion process in vivo.“The placenta has one of the body’s highest EGFR expression levels, and EGF is among the dominant factors regulating the proliferation, uterine [attachment], and fusion of human trophoblasts,” says Veiga-Lopez. “But other factors are involved as well. Our understanding of these processes is limited, as they are very difficult to study.”EGF likely plays a variety of roles throughout pregnancy.13,14,15 In the first trimester, EGF helps the developing placenta attach to the uterus. To nourish the rapidly growing fetus in later pregnancy stages, EGF and other factors primarily control the cell fusion process to keep up with the increasing complexity the villi—the finger-like structures that maximize the embryo’s contact with maternal blood.Any role of BPS in that fusion process is currently uncertain, says R. Michael Roberts, a professor emeritus of reproductive biology at the University of Missouri, who was not involved in the study. “The researchers proposed a new mechanism of action for BPS that is different from alterations of the classical steroid receptor pathway,” he says. “Although intriguing, I think it remains a hypothesis until confirmed by other studies at environmentally relevant doses.”Graham Burton, a professor emeritus of reproductive physiology at the University of Cambridge, United Kingdom, who also was not involved in the study, agrees with the authors’ conclusion that BPS blocks EGF-mediated cell fusion in vitro. However, extrapolating that finding to human pregnancies is difficult, he notes.“BPS may affect trophoblast proliferation early in the course of placental development, but I think it is less likely to affect in vivo syncytialization, as spontaneous fusion was not blocked in their experiments,” says Burton. “At the end of the day, we just don’t know enough about the role of EGF in regulating this complex process.”Recently generated organoid trophoblast cultures16,17 form structures similar to villi, differentiate into the STB and other cell types, and secrete placenta-specific peptides and hormones. These cultures closely resemble first-trimester placentas and may help clarify the regulation of cell fusion, says Burton.Silke Schmidt, PhD, writes about science, health, and the environment from Madison, Wisconsin.References1. Liao C, Liu F, Kannan K. 2012. Bisphenol S, a new bisphenol analogue, in paper products and currency bills and its association with bisphenol a residues. Environ Sci Technol 46(12):6515–6522, 10.1021/es300876n. Crossref, Medline, Google Scholar2. Björnsdotter MK, de Boer J, Ballesteros-Gómez A. 2017. Bisphenol A and replacements in thermal paper: a review. Chemosphere 182:691–706, PMID: 28528315, 10.1016/j.chemosphere.2017.05.070. Crossref, Medline, Google Scholar3. Liao C, Liu F, Alomirah H, Loi VD, Mohd MA, Moon H-B, et al.2012. Bisphenol S in urine from the United States and seven Asian countries: occurrence and human exposures. Environ Sci Technol 46(12):6860–6866, PMID: 22620267, 10.1021/es301334j. Crossref, Medline, Google Scholar4. Karrer C, Roiss T, von Goetz N, Gramec Skledar D, Peterlin Mašič L, Hungerbühler K, et al.2018. Physiologically based pharmacokinetic (PBPK) modeling of the bisphenols BPA, BPS, BPF, and BPAF with new experimental metabolic parameters: comparing the pharmacokinetic behavior of BPA with its substitutes. Environ Health Perspect 126(7):077002, PMID: 29995627, 10.1289/EHP2739. Link, Google Scholar5. 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Placenta 102:21–26, PMID: 33218574, 10.1016/j.placenta.2020.02.008. Crossref, Medline, Google Scholar9. Starkey RH, Cohen S, Orth DN. 1975. Epidermal growth factor: identification of a new hormone in human urine. Science 189(4205):800–802, PMID: 1172293, 10.1126/science.1172293. Crossref, Medline, Google Scholar10. NHANES (National Health and Nutrition Examination Survey).2016. 2013‐2014 Data Documentation, Codebook, and Frequencies. Personal Care and Consumer Product Chemicals and Metabolites (EPHPP_H). https://wwwn.cdc.gov/Nchs/Nhanes/2013-2014/EPHPP_H.htm [accessed 25 February 2021]. Google Scholar11. Kliman HJ, Nestler JE, Sermasi E, Sanger JM, Strauss JF. 1986. Purification, characterization, and in vitro differentiation of cytotrophoblasts from human term placentae. Endocrinology 118(4):1567–1582, PMID: 3512258, 10.1210/endo-118-4-1567. Crossref, Medline, Google Scholar12. Simán CM, Sibley CP, Jones CJ, Turner MA, Greenwood SL. 2001. The functional regeneration of syncytiotrophoblast in cultured explants of term placenta. Am J Physiol Regul Integr Comp Physiol 280(4):R1116–R1122, PMID: 11247834, 10.1152/ajpregu.2001.280.4.R1116. Crossref, Medline, Google Scholar13. Slowey MJ, Verhage HG, Fazleabas AT. 1994. Epidermal growth factor, transforming growth factor-alpha, and epidermal growth factor receptor localization in the baboon (Papio anubis) uterus during the menstrual cycle and early pregnancy. J Soc Gynecol Investig 1(4):277–284, PMID: 9419784, 10.1177/107155769400100406. Crossref, Medline, Google Scholar14. Dackor J, Caron KM, Threadgill DW. 2009. Placental and embryonic growth restriction in mice with reduced function epidermal growth factor receptor alleles. Genetics 183(1):207–218, PMID: 19564486, 10.1534/genetics.109.104372. Crossref, Medline, Google Scholar15. Fondacci C, Alsat E, Gabriel R, Blot P, Nessmann C, Evain-Brion D, et al.1994. Alterations of human placental epidermal growth factor receptor in intrauterine growth retardation. J Clin Invest 93(3):1149–1155, PMID: 8132754, 10.1172/JCI117067. Crossref, Medline, Google Scholar16. Turco MY, Gardner L, Kay RG, Hamilton RS, Prater M, Hollinshead MS, et al.2018. Trophoblast organoids as a model for maternal-fetal interactions during human placentation. Nature 564(7735):263–267, PMID: 30487605, 10.1038/s41586-018-0753-3. Crossref, Medline, Google Scholar17. Li Z, Kurosawa O, Iwata H. 2018. Development of trophoblast cystic structures from human induced pluripotent stem cells in limited-area cell culture. Biochem Biophys Res Commun 505(3):671–676, PMID: 30292409, 10.1016/j.bbrc.2018.09.181. Crossref, Medline, Google ScholarFiguresReferencesRelatedDetailsCited by Yue H, Tian Y, Wu X, Yang X, Xu P, Zhu H and Sang N (2023) Exploration of the damage and mechanisms of BPS exposure on the uterus and ovary of adult female mice, Science of The Total Environment, 10.1016/j.scitotenv.2023.161660, 868, (161660), Online publication date: 1-Apr-2023. Related articlesBisphenol S and Epidermal Growth Factor Receptor Signaling in Human Placental Cytotrophoblasts19 February 2021Environmental Health Perspectives Vol. 129, No. 6 June 2021Metrics About Article Metrics Publication History Manuscript received2 March 2021Manuscript accepted7 May 2021Originally published29 June 2021 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days." @default.
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