Bisphenol A impairs decidualization of human uterine stromal fibroblasts

Olson, Mark; Su, Ren-Wei; Flaws, Jodi A.; Fazleabas, Asgerally T.

doi:10.1016/j.reprotox.2017.07.008

Cited by 22 publications

(13 citation statements)

References 30 publications

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“…Particularly, BPA is able to influence ovarian morphology [6] and function, especially steroidogenesis [28][29][30][31][32][33][34] and folliculogenesis [32,[34][35][36], and, as well as uterine morphology [37] and function, especially uterine receptivity, consisting of the uterine ability to accommodate embryo attachment [38][39][40], and embryo implantation [37][38][39][40]. The impairment of endocrine function, and the consequent impairment of ovarian and uterine morphology and function, may lead to the development of several diseases involving reproductive system, especially ovary and uterus [19,41,42]. The ultimate consequence of the impairment of endocrine function and the morphology and function of the female reproductive system may be represented by female infertility.…”

Section: Introductionmentioning

confidence: 99%

Bisphenol A: an emerging threat to female fertility

Pivonello

Muscogiuri

Nardone

et al. 2020

Reprod Biol Endocrinol

178

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Bisphenol-A (BPA) has been reported to be associated to female infertility. Indeed, BPA has been found to be more frequently detected in infertile women thus leading to hypothesize a possible effect of BPA on natural conception and spontaneous fecundity. In addition, in procedures of medically assisted reproduction BPA exposure has been found to be negatively associated with peak serum estradiol levels during gonadotropin stimulation, number of retrieved oocytes, number of normally fertilized oocytes and implantation. BPA deleterious effects are more critical during perinatal exposure, causing dysregulation of hypothalamic-pituitary-ovarian axis in pups and adults, with a precocious maturation of the axis through a damage of GnRH pulsatility, gonadotropin signaling and sex steroid hormone production. Further, BPA exposure during early lifestage may have a transgenerational effect predisposing the subsequent generations to the risk of developing BPA related disease. Experimental studies suggested that prenatal, perinatal and postnatal exposure to BPA can impair several steps of ovarian development, induce ovarian morphology rearrangement and impair ovarian function, particularly folliculogenesis, as well as can impair uterus morphology and function, in female adult animal and offspring. Finally, studies carried out in animal models have been reported the occurrence of endometriosis-like lesions after BPA exposure. Moreover, BPA exposure has been described to encourage the genesis of PCOS-like abnormalities through the impairment of the secretion of sex hormones affecting ovarian morphology and functions, particularly folliculogenesis. The current manuscript summarizes the evidence regarding the association between BPA exposure and female infertility, reviewing both clinical and preclinical studies.

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Section: Introductionmentioning

confidence: 99%

Bisphenol A: an emerging threat to female fertility

Pivonello

Muscogiuri

Nardone

et al. 2020

Reprod Biol Endocrinol

178

View full text Add to dashboard Cite

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“…Upon in vitro exposure of human ESCs to 1 µM and 1 nM of BPA, there was an upregulation of ERα, ERβ, and PRA (Mannelli et al, 2015). However, exposure to doses of BPA higher than that reported in physiological biofluid concentrations (20 µg/ml) significantly reduced both ER and PR expressions in human uterine stromal fibroblast (HuF) cells undergoing decidualization (Olson, Su, Flaws, & Fazleabas, 2017), while only ERα was downregulated in the endometrium of mice exposed to 400 and 600 mg·kg·d of BPA during blastocyst implantation (Pan et al, 2015). This suggests that lower concentrations of BPA increase uterine levels of steroid hormones to promote decidualization while higher doses suppress their levels to impair decidualization.…”

Section: Effect Of Bpa On Steroid Hormones During Decidualizationmentioning

confidence: 99%

“…Exposure of decidualized HuF cells, isolated from the decidual parietalis of the placental membrane after normal vaginal delivery, to higher doses of BPA (10 and 20 μg/ml) for 8 days significantly downregulated messenger RNA (mRNA) expression of PRL, but not IGFBP1 mRNA levels (Olson et al, 2017). A similar effect was observed after the treatment of ESCs with a low dose (1 µM) of BPA for 24 hr (Mannelli et al, 2015).…”

Section: Effect Of Bpa On Decidualization Markersmentioning

confidence: 99%

Bisphenol A‐induced mechanistic impairment of decidualization

Nelson

Adu‐Gyamfi

Czika

et al. 2020

Molecular Reproduction Devel

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Decidualization is a crucial precedent to embryo implantation, as its impairment is a major contributor to female infertility and pregnancy complications. Unraveling the molecular mechanisms involved in the impairment of decidualization has been a subject of interest in the field of reproductive medicine. Evidence from several experimental settings show that exposure to bisphenol A (BPA), an endocrine‐disrupting chemical, affects the expression of several molecules that are involved in decidualization. Both low and high doses of BPA impair decidualization through the dysregulation of estrogen (ER) and progesterone (PR) receptors. Exposure to low doses of BPA leads to decreased levels and activities of several antioxidant enzymes, increased activity of endothelial nitric oxide synthase (eNOS), and increased production of nitric oxide (NO) via the upregulation of ER and PR. Consequently, oxidative stress is induced and decidualization becomes impaired. On the other hand, exposure to high doses of BPA downregulates ER and PR and impairs decidualization through two distinct pathways. One is through the upregulation of early growth response‐1 (EGR1) via increased phosphorylation of extracellular signal‐regulated protein kinases 1 and 2; and the other is through a reduced serum glucocorticoid‐induced kinase‐1 (SGK1)‐mediated downregulation of epithelial sodium channel‐α and the induction of oxidative stress. Thus, regardless of the dose, BPA can impair decidualization to trigger infertility and pregnancy complications. This warrants the need to adopt lifestyles that will decrease the tendency of getting exposed to BPA.

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“…Perinatal BPA exposure can alter the function of reproductive endocrine system by hypomethylating some imprinting genes during oocyte maturation or decreasing the expression of the estrogen receptor ER at both the mRNA and protein levels [21]. The direct toxicity of BPA is manifested in the disruption of decidualization in vitro [22], enhanced expression of estrogen receptors-α (ER-α) and oxidative stress in embryonic stem cells [23], and promotion of apoptosis [24].…”

Section: Introductionmentioning

confidence: 99%

Bisphenol-A Dose-dependently Regulates The Development of Ovary and Uterus through Differential Expression of METTL3

Zhang

Zhu

Zhang

et al. 2020

Preprint

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Background: Environmental endocrine disruptors, which have a profound impact on the reproductive system, can cause endocrine and reproductive disorders, such as polycystic ovary syndrome (PCOS). Bisphenol-A (BPA) is a common endocrine disruptor which can affect the function of the reproductive system under low-dose conditions. However, the mechanism by which this molecule disrupts normal reproduction is still unclear. In this study, we investigated the effects of BPA on the RNA methyltransferase METTL3 in adolescent female rats which may be a possible mode of action of BPA. Methods: 4-week-old Sprague-Dawley (SD) rats were intragastrically treated for 10 weeks, which were divided into blank group (n = 8), control group (soybean oil, n = 8), three BPA-treatment groups (0.5 mg/kg BPA + soybean oil, 5 mg/kg BPA + soybean oil, 50 mg/kg BPA + soybean oil, n = 8). Results: The results showed that low-dose BPA (0.5 mg/kg) increased the coefficient of uteri and ovaries, and promoted the growth of uteri in rats without causing hyperandrogenism and ovarian polycystic changes. Oral BPA disturbed the expression of CYP17A1, CYP11A1 and METTL3 in ovaries and effected the level of serum testosterone. Conclusions: Our results suggested that oral BPA might interfere uterine and ovarian morphology and the level of hormone with RNA methylation by disturbing the expression level of METTL3. RNA methylation will be a new way to explain the interference mechanism of BPA.

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Bisphenol A impairs decidualization of human uterine stromal fibroblasts

Cited by 22 publications

References 30 publications

Bisphenol A: an emerging threat to female fertility

Bisphenol A: an emerging threat to female fertility

Bisphenol A‐induced mechanistic impairment of decidualization

Bisphenol-A Dose-dependently Regulates The Development of Ovary and Uterus through Differential Expression of METTL3

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