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National Institute of Environmental Health Sciences

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Publication Detail

Title: Supraphysiological Concentrations of Bisphenol A Alter the Expression of Extracellular Vesicle-Enriched miRNAs From Human Primary Granulosa Cells.

Authors: Rodosthenous, Rodosthenis S; Baccarelli, Andrea A; Mansour, Abdallah; Adir, Michal; Israel, Ariel; Racowsky, Catherine; Hauser, Russ; Bollati, Valentina; Machtinger, Ronit

Published In Toxicol Sci, (2019 05 01)

Abstract: Bisphenol A (BPA) is a widely used chemical that has been detected in follicular fluid and associated with adverse reproductive effects. Granulosa cells have an important role in follicular growth and oocyte maturation, however, little is known about the biological mechanisms of BPA toxicity on human granulosa cells. In this study, we exposed primary granulosa cells to different concentrations of BPA (0, 20, 200, 2000, and 20 000 ng/ml) and used quantitative polymerase chain reaction to measure the expression levels of miRNAs enriched in extracellular vesicles (EV-enriched miRNAs), and cellular levels of selected target genes of differentially expressed EV-enriched miRNAs. We found that exposure to 20 000 ng/ml BPA was associated with decreased levels of EV-miR-27b-3p (FC = 0.58, p = .04) and increased levels of its biologically relevant target genes FADD (FC = 1.22, p = .01), IGF1 (FC = 1.59, p = .06), and PPARG (FC = 1.73, p = .001) as compared with the control. In addition, we observed that under the same exposure conditions, the expression levels of miR-27b-3p in granulosa cells were also downregulated (FC = 0.65, p = .03) as compared with the control. Our findings suggest that both cellular and extracellular changes in gene expression may mediate BPA toxicity in granulosa cells.

PubMed ID: 30690568 Exiting the NIEHS site

MeSH Terms: Adult; Benzhydryl Compounds/toxicity*; Cells, Cultured; Dose-Response Relationship, Drug; Endocrine Disruptors/toxicity*; Extracellular Vesicles/drug effects*; Extracellular Vesicles/genetics; Extracellular Vesicles/metabolism; Fas-Associated Death Domain Protein/genetics; Fas-Associated Death Domain Protein/metabolism; Female; Gene Expression Regulation, Developmental; Granulosa Cells/drug effects*; Granulosa Cells/metabolism; Humans; Insulin-Like Growth Factor I/genetics; Insulin-Like Growth Factor I/metabolism; MicroRNAs/genetics; MicroRNAs/metabolism*; Oogenesis/drug effects*; Oogenesis/genetics; PPAR gamma/genetics; PPAR gamma/metabolism; Phenols/toxicity*; Primary Cell Culture; Risk Assessment

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