Please use this identifier to cite or link to this item: http://bura.brunel.ac.uk/handle/2438/20293
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dc.contributor.authorde Aguiar Greca, S-C-
dc.contributor.authorKyrou, I-
dc.contributor.authorPink, R-
dc.contributor.authorRandeva, H-
dc.contributor.authorGrammatopoulos, D-
dc.contributor.authorSilva, E-
dc.contributor.authorKarteris, E-
dc.date.accessioned2020-02-14T13:36:03Z-
dc.date.available2020-02-03-
dc.date.available2020-02-14T13:36:03Z-
dc.date.issued2020-02-03-
dc.identifier.citationde Aguiar Greca, S.-C.; Kyrou, I.; Pink, R.; Randeva, H.; Grammatopoulos, D.; Silva, E.; Karteris, E. Involvement of the Endocrine-Disrupting Chemical Bisphenol A (BPA) in Human Placentation. J. Clin. Med. 2020, 9, 405.en_US
dc.identifier.issn2077-0383-
dc.identifier.urihttp://bura.brunel.ac.uk/handle/2438/20293-
dc.description.abstractBackground: Endocrine-disrupting chemicals (EDCs) are environmental chemicals/toxicants that humans are exposed to, interfering with the action of multiple hormones. Bisphenol A (BPA) is classified as an EDC with xenoestrogenic activity with potentially adverse effects in reproduction. Currently, a significant knowledge gap remains regarding the complete spectrum of BPA-induced effects on the human placenta. As such, the present study examined the effects of physiologically relevant doses of BPA in vitro. Methods: qRT-PCR, Western blotting, immunofluorescence, ELISA, microarray analyses, and bioinformatics have been employed to study the effects of BPA using nonsyncytialised (non-ST) and syncytialised (ST) BeWo cells. Results: Treatment with 3 nM BPA led to an increase in cell number and altered the phosphorylation status of p38, an effect mediated primarily via the membrane-bound estrogen receptor (GPR30). Nonbiased microarray analysis identified 1195 and 477 genes that were differentially regulated in non-ST BeWo cells, whereas in ST BeWo cells, 309 and 158 genes had altered expression when treated with 3 and 10 nM, respectively. Enriched pathway analyses in non-ST BeWo identified a leptin and insulin overlap (3 nM), methylation pathways (10 nM), and differentiation of white and brown adipocytes (common). In the ST model, most significantly enriched were the nuclear factor erythroid 2-related factor 2 (NRF2) pathway (3 nM) and mir-124 predicted interactions with cell cycle and differentiation (10 nM). Conclusion: Collectively, our data offer a new insight regarding BPA effects at the placental level, and provide a potential link with metabolic changes that can have an impact on the developing fetus.en_US
dc.description.sponsorshipIsambard PhD Scholarship, Brunel University Londonen_US
dc.format.extent1 - 24 (24)-
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.subjectEndocrine-disrupting chemicalsen_US
dc.subjectBPAen_US
dc.subjectPlacentaen_US
dc.subjectMicroarrayen_US
dc.titleInvolvement of the Endocrine-Disrupting Chemical Bisphenol A (BPA) in Human Placentationen_US
dc.typeArticleen_US
dc.identifier.doihttp://dx.doi.org/10.3390/jcm9020405-
dc.relation.isPartOfJournal of Clinical Medicine-
pubs.issue2-
pubs.publication-statusPublished online-
pubs.volume9-
Appears in Collections:Dept of Life Sciences Research Papers

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