ESTROGEN-REGULATED miRNA-27b IS ALTERED BY BISPHENOL A IN ENDOMETRIAL STROMAL CELLS

Reed, Berenice; Babayev, Samir; Chen, Lucy X.; Carr, Bruce R.; Word, R. Ann; Jimenez, Patricia T.

doi:10.1530/rep-18-0041

Cited by 30 publications

(24 citation statements)

References 63 publications

(72 reference statements)

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“…The addition of ZEA and BPA also altered miRNA expression although these changes were not as remarkable as in the case of E2. Our results are in agreement with previous studies where BPA and ZEA altered miRNA expression in several other cell lines [ 20 , 60 , 61 , 62 , 63 ]. The observation that the effect of E2 on the expression of miR200s and miR203a was decreased by MPP, an ERα-selective antagonist, supports the presumption that ERα is involved in the regulation of these miRNAs.…”

Section: Discussionsupporting

confidence: 94%

The Cell-Free Expression of MiR200 Family Members Correlates with Estrogen Sensitivity in Human Epithelial Ovarian Cells

Márton

Varga

Széles

et al. 2020

IJMS

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Exposure to physiological estrogens or xenoestrogens (e.g., zearalenone or bisphenol A) increases the risk for cancer. However, little information is available on their significance in ovarian cancer. We present a comprehensive study on the effect of estradiol, zearalenone and bisphenol A on the phenotype, mRNA, intracellular and cell-free miRNA expression of human epithelial ovarian cell lines. Estrogens induced a comparable effect on the rate of cell proliferation and migration as well as on the expression of estrogen-responsive genes (GREB1, CA12, DEPTOR, RBBP8) in the estrogen receptor α (ERα)-expressing PEO1 cell line, which was not observable in the absence of this receptor (in A2780 cells). The basal intracellular and cell-free expression of miR200s and miR203a was higher in PEO1, which was accompanied with low ZEB1 and high E-cadherin expression. These miRNAs showed a rapid but intermittent upregulation in response to estrogens that was diminished by an ERα-specific antagonist. The role of ERα in the regulation of the MIR200B-MIR200A-MIR429 locus was further supported by publicly available ChIP-seq data. MiRNA expression of cell lysates correlated well with cell-free miRNA expression. We conclude that cell-free miR200s might be promising biomarkers to assess estrogen sensitivity of ovarian cells.

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Section: Discussionsupporting

confidence: 94%

The Cell-Free Expression of MiR200 Family Members Correlates with Estrogen Sensitivity in Human Epithelial Ovarian Cells

Márton

Varga

Széles

et al. 2020

IJMS

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“…Likewise, they revealed that BPA could decrease miR‐324. Moreover, the study of Reed et al showed a mechanism that BPA impairs miR‐27b levels thereby leading to changes in normal vasculogenesis and endometrial angiogenesis (Reed et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

A systematic review of microRNA expression studies with exposure to bisphenol A

Farahani

Rezaei‐Tavirani

Arjmand

2020

J of Applied Toxicology

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Bisphenol A (BPA), as a common industrial component, is generally consumed in the synthesis of polymeric materials. To gain a deeper understanding of the detrimental effects of BPA, BPA-induced microRNA (miRNA) alterations were investigated. A systematic search was performed in the PubMed, SCOPUS and Web of Science databases to evoke relevant published data up to August 10, 2019. We identified altered miRNAs that have been repeated in at least three studies. Moreover, miRNA homology analysis between human and nonhuman species was performed to determine the toxicity signatures of BPA in human exposure. In addition, to reflect the effects of environmental exposure levels of BPA, the study designs were categorized into two groups, including low and high doses according to the previous definitions. In total, 28 studies encountered our criteria and 17 miRNAs were identified that were differentially expressed in at least three independent studies. Upregulating miR-146a and downregulating miR-192, miR-134, miR-27b and miR-324 were found in three studies. MiR-122 and miR-29a were upregulated in four studies after BPA exposure, and miR-21 was upregulated in six studies. The results indicate that BPA at low-level exposures can also alter miRNA expression in response to toxicity. Finally, the miRNA-related pathways showed that BPA seriously can affect human health through various cell signaling pathways, which were predictable and consistent with existing studies. Overall, our findings suggest that further studies should be conducted to examine the role of miRNA level changes in human BPA exposure.

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“…Indeed, a bioinformatics analysis carried out using two different prediction algorithms (miRDB and TargetScan) allowed us to identify about 27 microRNAs that have Pparγ as their target gene. Among these, we searched those microRNAs whose expression can be affected by exposure to BPA [87][88][89][90][91]. Following this intersection, two candidate microRNAs, microRNA 27a and 27b, were selected from the above-mentioned list.…”

Section: Discussionmentioning

confidence: 99%

Low-dose Bisphenol-A Promotes Epigenetic Changes at Pparγ Promoter in Adipose Precursor Cells

et al. 2020

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Exposure to endocrine-disrupting chemicals such as Bisphenol-A (BPA) is associated with an increase in obesity prevalence. Diet is the primary cause of human exposure to this contaminant. BPA promotes obesity by inducing adipocyte dysfunction and altering adipogenesis. Contradictory evidence and unanswered questions are reported in the literature concerning the BPA effects on adipogenesis. To clarify this issue, we tested the effects of prolonged low-dose BPA exposure on different phases of adipogenesis in committed 3T3L1 and uncommitted NIH3T3 preadipocytes. Our findings show that BPA effects on the adipogenesis are mediated by epigenetic mechanisms by reducing peroxisome proliferator-activated receptor gamma (Pparγ) promoter methylation in preadipocytes. Nevertheless, in BPA-exposed 3T3L1, Pparγ expression only transiently increases as lipid accumulation at day 4 of differentiation, without altering the adipogenic potential of the precursor cells. In the absence of differentiation mix, BPA does not make the 3T3L1 an in vitro model of spontaneous adipogenesis and the effects on the Pparγ expression are still limited at day 4 of differentiation. Furthermore, BPA exposure does not commit the NIH3T3 to the adipocyte lineage, although Pparγ overexpression is more evident both in preadipocytes and during the adipocyte differentiation. Interestingly, termination of the BPA exposure restores the Pparγ promoter methylation and inflammatory profile of the 3T3L1 cells. This study shows that BPA induces epigenetic changes in a key adipogenic gene. These modifications are reversible and do not affect preadipocyte commitment and/or differentiation. We identify an alternative transcriptional mechanism by which BPA affects gene expression and demonstrate how the challenge of preventing exposure is fundamental for human health.

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ESTROGEN-REGULATED miRNA-27b IS ALTERED BY BISPHENOL A IN ENDOMETRIAL STROMAL CELLS

Cited by 30 publications

References 63 publications

The Cell-Free Expression of MiR200 Family Members Correlates with Estrogen Sensitivity in Human Epithelial Ovarian Cells

The Cell-Free Expression of MiR200 Family Members Correlates with Estrogen Sensitivity in Human Epithelial Ovarian Cells

A systematic review of microRNA expression studies with exposure to bisphenol A

Low-dose Bisphenol-A Promotes Epigenetic Changes at Pparγ Promoter in Adipose Precursor Cells

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