Effects of Prenatal Environmental Exposures on the Development of Endometriosis in Female Offspring

Wei, Ming; Chen, Xinyuan; Zhao, Ye; Cao, Baoli; Zhao, Wenli

doi:10.1177/1933719116630418

Cited by 18 publications

(16 citation statements)

References 94 publications

(118 reference statements)

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“…They are known endocrine disrupters, with estrogenic and antiandrogenic effects including delayed time to pregnancy. 70 Exposure to environmental toxins during the prenatal period is thought to have the greatest effect on reproduction and endometriosis, 71 and elevated serum phthalates in women are associated with endometriosis. 72,73 However, our search could not locate any publications on the specific effect of environmental pollutants or other environmental factors on endometrial stem/progenitor cells.…”

Section: Environmentmentioning

confidence: 99%

Cellular Origins of Endometriosis: Towards Novel Diagnostics and Therapeutics

et al. 2020

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Endometriosis remains an enigmatic disease of unknown etiology, with delayed diagnosis and poor therapeutic options. This review will discuss the cellular, physiological, and genomic evidence of Sampson's hypothesis of retrograde menstruation as a cause of pelvic endometriosis and as the basis of phenotypic heterogeneity of the disease. We postulate that collaborative research at the single cell level focused on unlocking the cellular, physiological, and genomic mechanisms of endometriosis will be accompanied by advances in personalized diagnosis and therapies that target unique subtypes of endometriosis disease. These advances will address the clinical conundrums of endometriosis clinical care—including diagnostic delay, suboptimal treatments, disease recurrence, infertility, chronic pelvic pain, and quality of life. There is an urgent need to improve outcomes for women with endometriosis. To achieve this, it is imperative that we understand which cells form the lesions, how they arrive at distant sites, and what factors govern their ability to survive and invade at ectopic locations. This review proposes new research avenues to address these basic questions of endometriosis pathobiology that will lay the foundations for new diagnostic tools and treatment pathways.

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Section: Environmentmentioning

confidence: 99%

Cellular Origins of Endometriosis: Towards Novel Diagnostics and Therapeutics

et al. 2020

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“…Several studies have highlighted the negative effects of BPA on reproductive system [17]. Particularly, it has been shown that BPA displays a high affinity for ER, having an estrogen-mimicking behavior and consequently stimulating estrogen function [11][12][13]; therefore, BPA has been hypothesized to be involved in several diseases of female reproductive system [3,[18][19][20][21][22], due to its property to stimulate ER-dependent gene expression involved in the pathophysiology of female reproductive system [23][24][25][26]. Moreover, BPA is also able to inhibit androgen function by binding AR [27].…”

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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“…PCBs may inhibit the activity of human estrogen sulfotransferase, an estrogen-degrading enzyme (Kester et al 2000), thereby increasing the secretion of estrogen and the risk of hormone-dependent diseases. Accumulating evidence had suggested that higher PCBs exposure may increase the risk of endometriosis (Hu et al 2018;Martinez-Zamora et al 2015;Porpora et al 2006;Wei et al 2016). A reduced responsiveness to progesterone and overexpression of matrix metalloproteinases may be a key element of endometrial dysfunction associated with endometriosis (Osteen et al 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Intrauterine exposure to an adverse environment will not only affect fetal development and lead to unfavorable pregnancy outcomes, but it will also have long-term impacts on disease susceptibility into late adulthood (Barker 1997;Godfrey and Barker 2001), including endometriosis (Wei et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Prenatal polychlorinated biphenyl exposure promotes invasion of progeny ectopic endometrial stromal cells via epigenetic modification of EZH2

Wang¹,

Ye²,

Hu³

et al. 2021

Preprint

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Polychlorinated biphenyls(PCBs) are persistent environmental endocrine disruptor. This study aim to investigate the changes of the ectopic endometrium invasive ability and the possible mechanism after exposure to PCBs during pregnancy. In total, 12 female Sprague Dawley rats were intraperitoneally injected with Aroclor 1221 (1 mg/kg) or dimethyl sulfoxide (1 mg/kg) at 16 and 18 days of gestation. The endometriosis model was established by autogenous uterine abdominal wall implantation 2 months after birth. The degree of adhesion between the endometriosis and the greater omentum, as well as cell morphology and Transwell invasion patterns were used to evaluate the invasive ability of progeny ectopic endometrial stromal cells (ESCs). Moreover, the effect of the enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2)/ trimethylation of Histone 3 lysine 27 (H3K27me3) axis was examined using a highly selective EZH2 inhibitor, GSK126. After gestational PCBs exposure, the adhesion between the endometrium and the greater omentum was enhanced (P<0.05), and the length and number of microvilli were significantly increased (P<0.01). Exposure to PCBs during pregnancy increased the invasive ability of the ectopic ESCs (P<0.01), with upregulated expression levels of EZH2 and H3k27me3, which were abrogated by the EZH2 inhibitor GSK126. In conclusion, exposure to PCBs during pregnancy increased the invasive ability of the ectopic endometrium, which may be mediated by EZH2.

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Effects of Prenatal Environmental Exposures on the Development of Endometriosis in Female Offspring

Cited by 18 publications

References 94 publications

Cellular Origins of Endometriosis: Towards Novel Diagnostics and Therapeutics

Cellular Origins of Endometriosis: Towards Novel Diagnostics and Therapeutics

Bisphenol A: an emerging threat to female fertility

Prenatal polychlorinated biphenyl exposure promotes invasion of progeny ectopic endometrial stromal cells via epigenetic modification of EZH2

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