ArticleEnvironmental health perspectives2011
Low concentrations of bisphenol A induce mouse spermatogonial cell proliferation by G protein-coupled receptor 30 and estrogen receptor-α.
Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 112 citations in OpenAlex.
- Estrogen Receptors-Mediated Apoptosis in Hormone-Dependent Cancers.International journal of molecular sciences · 2022Review
- Characterization of Estrogenic Activity and Site-Specific Accumulation of Bisphenol-A in Epididymal Fat Pad: Interfering Effects on the Endocannabinoid System and Temporal Progression of Germ Cells.International journal of molecular sciences · 2021Article
- Detrimental Effects of Bisphenol Compounds on Physiology and Reproduction in Fish: A Literature Review.Environmental toxicology and pharmacology · 2021Review
- Putative adverse outcome pathways for female reproductive disorders to improve testing and regulation of chemicals.Archives of toxicology · 2020Review
- Review
- GPER as a Receptor for Endocrine-Disrupting Chemicals (EDCs).Frontiers in endocrinology · 2020Review
- A Cell-Based Method to Detect Agonist and Antagonist Activities of Endocrine-Disrupting Chemicals on GPER.Frontiers in endocrinology · 2020Article
- CLARITY-BPA academic laboratory studies identify consistent low-dose Bisphenol A effects on multiple organ systems.Basic & clinical pharmacology & toxicology · 2019Review
- Melatonin inhibits the proliferation of breast cancer cells induced by bisphenol A via targeting estrogen receptor-related pathways.Thoracic cancer · 2018Article
- Calycosin inhibits the in vitro and in vivo growth of breast cancer cells through WDR7-7-GPR30 Signaling.Journal of experimental & clinical cancer research : CR · 2017Article
- Bisphenol A Affects on the Functional Properties and Proteome of Testicular Germ Cells and Spermatogonial Stem Cells in vitro Culture Model.Scientific reports · 2017Article
- Endocrine-disrupting chemicals and uterine fibroids.Fertility and sterility · 2016Review
- GPER-novel membrane oestrogen receptor.Clinical science (London, England : 1979) · 2016Review
- Response to "Comment on 'Effects of Atrazine on Estrogen Receptor 〈- and G Protein-Coupled Receptor 30-Mediated Signaling and Proliferation in Cancer Cells and Cancer-Associated Fibroblasts'".Environmental health perspectives · 2016Article
- Neonatal bisphenol A exposure induces meiotic arrest and apoptosis of spermatogenic cells.Oncotarget · 2016Article
- EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals.Endocrine reviews · 2015Review
- International Union of Basic and Clinical Pharmacology. XCVII. G Protein-Coupled Estrogen Receptor and Its Pharmacologic Modulators.Pharmacological reviews · 2015Review
- Non-monotonic dose responses in studies of endocrine disrupting chemicals: bisphenol a as a case study.Dose-response : a publication of International Hormesis Society · 2014Article
- Rapamycin inhibits acrolein-induced apoptosis by alleviating ROS-driven mitochondrial dysfunction in male germ cells.Cell proliferation · 2014Article
- Bisphenol A induces differentiation of human preadipocytes in the absence of glucocorticoid and is inhibited by an estrogen-receptor antagonist.Nutrition & diabetes · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundBisphenol A (BPA) is one of the most prevalent chemicals in daily-use materials; therefore, human exposure to BPA is ubiquitous. The estrogenicity of BPA is generally mediated by nuclear estrogen receptors (ERs). However, low concentrations of BPA stimulate seminoma cell proliferation by an uncertain mechanism that does not involve activation of ERs.
objectiveWe investigated the possible promoting effects of low-concentration BPA and the possible mechanism(s) using the murine ER-β negative spermatogonial GC-1 cell line. METHODS AND
resultsUsing the specific signaling inhibitor, BPA at test concentrations ranging from 10-10 to 10-8 M markedly induced proliferation of GC-1 cells by activating both cGMP-dependent protein kinase (PKG) and epidermal growth factor receptor (EGFR) extracellular regulated kinase (ERK) pathways. BPA stimulated a rapid (15-min) phosphorylation of the transcription factor cAMP response element binding protein (CREB) and the cell cycle regulator retinoblastoma protein (Rb). Interestingly, ER-α phosphorylation is involved in the proliferation, whereas BPA does not directly transactivate ER-α in gene reporter assays. Using specific agonists and gene silencing, we further observed that BPA mediates the proliferation and fos gene expression of GC-1 cells by G protein-coupled receptor 30 (GPR30) and ER-α.
conclusionsOur data suggest that low concentrations of BPA activate the PKG and EGFR/ERK/c-fos pathways through a cross-talk between GPR30 and ER-α, which in turn stimulates GC-1 cell proliferation. The present study provides a novel insight regarding the potential role of GPR30 and ER-α in mediating the proliferative effects of BPA in male germ cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.