Environmental Estrogens and Their Biological Effects through GPER Mediated Signal Pathways

Qie, Yu; Qin, Weiping; Zhao, Keda; Liu, Chang; Zhao, Lingjuan; Guo, Liang-Hong

doi:10.1016/j.envpol.2021.116826

Cited by 36 publications

(16 citation statements)

References 135 publications

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“…As G1 and BPA effects were abolished in the presence of an ER antagonist, after ER knockdown and in islets cells from BERKO mice, we suggest that ERα and ERβ are responsible for the effect of GPER activation. A crosstalk between GPER and ERα has been described for E2 and environmental estrogens (Qie et al, 2021). Remarkably, E2, which also binds to and activates GPER (Revankar et al, 2005; Thomas et al, 2005), does not behave as G1 or BPA.…”

Section: Discussionmentioning

confidence: 99%

G protein-coupled estrogen receptor activation by Bisphenol-A disrupts protection from apoptosis conferred by estrogen receptors ERα and ERβ in pancreatic beta cells

Babiloni-Chust

Santos

Medina-Gali

et al. 2022

Preprint

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Aims/hypothesis: 17β-oestradiol protects pancreatic beta cells from apoptosis via the oestrogen receptor α (ERα) and β (ERβ), and the G protein-coupled oestrogen receptor (GPER/GPR30). Conversely, the endocrine disruptor Bisphenol-A (BPA), which exerts multiple effects in beta cells via the same oestrogen receptors, increased basal apoptosis. We investigated the molecular initiated events underlying these opposite actions. Methods: Apoptosis was determined by nuclear dyes, flow cytometry and luminescence. Oestrogen receptors were inhibited by small interfering RNAs. ERα and ERβ heterodimers were studied by molecular dynamics simulations, proximity ligand assay and co-immunoprecipitation. All experiments were performed in rat INS-1E and human EndoC-βH1 cells and dispersed islet cells from wild-type and ERβ knockout mice. Results: BPA exposure induced reactive oxygen species production and induced apoptosis. GPER agonist G1 also induced apoptosis, but to a less extent than BPA. Either gene downregulation or pharmacological inhibition of each receptor resulted in augmented beta cell apoptosis in the absence of external stimuli. BPA- and G1-induced apoptosis was abolished in ERα-, ERβ- and GPER-silenced cells as well as in dispersed islet cells from ERβ knockout mice. Moreover, pharmacological blockade of each receptor also abrogated BPA- and G1-induced apoptosis. ERα and ERβ pharmacological agonists had no effect on beta cell viability. BPA interaction with ERα and ERβ as well as GPER activation by G1 or BPA decreased ERαβ heterodimerization. Conclusions/interpretation: Our data suggest that ERα, ERβ and GPER play a key role in beta cell survival, where BPA-induced changes in GPER activation as well as in ERαβ heterodimer formation may increase beta cell apoptosis.

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Section: Discussionmentioning

confidence: 99%

G protein-coupled estrogen receptor activation by Bisphenol-A disrupts protection from apoptosis conferred by estrogen receptors ERα and ERβ in pancreatic beta cells

Babiloni-Chust

Santos

Medina-Gali

et al. 2022

Preprint

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“…However, on the whole, the long-term social project of environmental pollution control needs to be adhered to for a long time in the aspect of pollution control. This study starts with the characteristics and impact factors of environmental pollution to explore long-term pollution control measures [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Using Sociological Theories and Methods to Analyze the Solutions and Measures of Environmental Pollution Problems

Su-qin

2022

Journal of Environmental and Public Health

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In order to further improve the effectiveness of environmental pollution control and improve the quality of the atmospheric ecological environment, this article discusses regional environmental pollution control from the perspective of sociological theories and methods. Therefore, the article starts with the characteristics of environmental air pollution, combined with linear regression analysis and PSR model principal component analysis, focuses on the impact factors of environmental pollution, and concludes that the weights of pressure layer, state layer, and response layer for the impact of environmental state are 0.4824, 0.261, and 0.1207, respectively. On this basis, from the perspective of social, collaborative governance, and public management, this article focuses on the political measures of environmental pollution.

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“…These concentrations are lower than those necessary to stimulate nuclear ERs [ 136 ]. The G protein-coupled estrogen receptor is a mER that plays a major role in BPA-induced toxicity [ 137 ].…”

Section: Effects Of Bpa Exposure On Different Body Systemsmentioning

confidence: 99%

Natural Products in Mitigation of Bisphenol A Toxicity: Future Therapeutic Use

et al. 2022

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Bisphenol A (BPA) is a ubiquitous environmental toxin with deleterious endocrine-disrupting effects. It is widely used in producing epoxy resins, polycarbonate plastics, and polyvinyl chloride plastics. Human beings are regularly exposed to BPA through inhalation, ingestion, and topical absorption routes. The prevalence of BPA exposure has considerably increased over the past decades. Previous research studies have found a plethora of evidence of BPA’s harmful effects. Interestingly, even at a lower concentration, this industrial product was found to be harmful at cellular and tissue levels, affecting various body functions. A noble and possible treatment could be made plausible by using natural products (NPs). In this review, we highlight existing experimental evidence of NPs against BPA exposure-induced adverse effects, which involve the body’s reproductive, neurological, hepatic, renal, cardiovascular, and endocrine systems. The review also focuses on the targeted signaling pathways of NPs involved in BPA-induced toxicity. Although potential molecular mechanisms underlying BPA-induced toxicity have been investigated, there is currently no specific targeted treatment for BPA-induced toxicity. Hence, natural products could be considered for future therapeutic use against adverse and harmful effects of BPA exposure.

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Environmental Estrogens and Their Biological Effects through GPER Mediated Signal Pathways

Cited by 36 publications

References 135 publications

G protein-coupled estrogen receptor activation by Bisphenol-A disrupts protection from apoptosis conferred by estrogen receptors ERα and ERβ in pancreatic beta cells

G protein-coupled estrogen receptor activation by Bisphenol-A disrupts protection from apoptosis conferred by estrogen receptors ERα and ERβ in pancreatic beta cells

[Retracted] Using Sociological Theories and Methods to Analyze the Solutions and Measures of Environmental Pollution Problems

Natural Products in Mitigation of Bisphenol A Toxicity: Future Therapeutic Use

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