ArticlePLoS genetics2017
G protein-coupled estrogen receptor regulates embryonic heart rate in zebrafish.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 57 citations in OpenAlex.
- Exposure to nitrate and nitrite disrupts cardiovascular development through estrogen receptor in zebrafish embryos and larvae.Fish physiology and biochemistry · 2024Article
- Testosterone acts through the membrane protein GPRC6A to cause cardiac edema in zebrafish embryos.Development (Cambridge, England) · 2024Article
- Hemato-vascular specification requires arnt1 and arnt2 genes in zebrafish embryos.Development (Cambridge, England) · 2023Article
- Article
- G protein-coupled estrogen receptor 1 regulates renal endothelin-1 signaling system in a sex-specific manner.Frontiers in physiology · 2023Article
- Zebrafish as an emerging model to study estrogen receptors in neural development.Frontiers in endocrinology · 2023Review
- Emerging Roles for G Protein-Coupled Estrogen Receptor 1 in Cardio-Renal Health: Implications for Aging.Biomolecules · 2022Review
- Application of Transgenic Zebrafish Models for Studying the Effects of Estrogenic Endocrine Disrupting Chemicals on Embryonic Brain Development.Frontiers in pharmacology · 2022Review
- The Interface of Nuclear and Membrane Steroid Signaling.Endocrinology · 2021Review
- Embryonic Onset of Sexually Dimorphic Heart Rates in the Viviparous Fish,Biomedicines · 2021Article
- Estrogen accelerates heart regeneration by promoting the inflammatory response in zebrafish.The Journal of endocrinology · 2020Article
- GPER as a Receptor for Endocrine-Disrupting Chemicals (EDCs).Frontiers in endocrinology · 2020Review
- Differential activity of BPA, BPAF and BPC on zebrafish estrogen receptors in vitro and in vivo.Toxicology and applied pharmacology · 2019Article
- ahr2, But Not ahr1a or ahr1b, Is Required for Craniofacial and Fin Development and TCDD-dependent Cardiotoxicity in Zebrafish.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- G Protein-Coupled Estrogen Receptor Is Not Required for Sex Determination or Ovary Function in Zebrafish.Endocrinology · 2018Article
- The Primodos components Norethisterone acetate and Ethinyl estradiol induce developmental abnormalities in zebrafish embryos.Scientific reports · 2018Article
- Brain Aromatase Modulates Serotonergic Neuron by Regulating Serotonin Levels in Zebrafish Embryos and Larvae.Frontiers in endocrinology · 2018Article
- Modeling Sex-Bias in Anxiety: Pros and Cons of a Larval Zebrafish Model.Chronic stress (Thousand Oaks, Calif.)Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Estrogens act by binding to estrogen receptors alpha and beta (ERα, ERβ), ligand-dependent transcription factors that play crucial roles in sex differentiation, tumor growth and cardiovascular physiology. Estrogens also activate the G protein-coupled estrogen receptor (GPER), however the function of GPER in vivo is less well understood. Here we find that GPER is required for normal heart rate in zebrafish embryos. Acute exposure to estrogens increased heart rate in wildtype and in ERα and ERβ mutant embryos but not in GPER mutants. GPER mutant embryos exhibited reduced basal heart rate, while heart rate was normal in ERα and ERβ mutants. We detected gper transcript in discrete regions of the brain and pituitary but not in the heart, suggesting that GPER acts centrally to regulate heart rate. In the pituitary, we observed gper expression in cells that regulate levels of thyroid hormone triiodothyronine (T3), a hormone known to increase heart rate. Compared to wild type, GPER mutants had reduced levels of T3 and estrogens, suggesting pituitary abnormalities. Exposure to exogenous T3, but not estradiol, rescued the reduced heart rate phenotype in gper mutant embryos, demonstrating that T3 acts downstream of GPER to regulate heart rate. Using genetic and mass spectrometry approaches, we find that GPER regulates maternal estrogen levels, which are required for normal embryonic heart rate. Our results demonstrate that estradiol plays a previously unappreciated role in the acute modulation of heart rate during zebrafish embryonic development and suggest that GPER regulates embryonic heart rate by altering maternal estrogen levels and embryonic T3 levels.
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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.