Evidence map›Paper›PMID 26998610›Full record

ArticlePloS one2016

Characterisation of Signalling by the Endogenous GPER1 (GPR30) Receptor in an Embryonic Mouse Hippocampal Cell Line (mHippoE-18).

Nicholas J Evans, Asha L Bayliss, Vincenzina Reale, Peter D Evans

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  3. Review
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  6. From Menopause to Neurodegeneration-Molecular Basis and Potential Therapy.International journal of molecular sciences · 2021
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  10. The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020
    Review
  11. Article
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  13. Review
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  15. Review
  16. Pioglitazone, a PPAR-γ Activator, Stimulates BKFrontiers in pharmacology · 2018
    Article
  17. Genes linked to species diversity in a sexually dimorphic communication signal in electric fish.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2018
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Nicholas J EvansThe Signalling Laboratory, The Babraham Institute, Cambridge, CB22 3AT, United Kingdom.
Asha L BaylissThe Signalling Laboratory, The Babraham Institute, Cambridge, CB22 3AT, United Kingdom.
Vincenzina RealeThe Signalling Laboratory, The Babraham Institute, Cambridge, CB22 3AT, United Kingdom.
Peter D EvansThe Signalling Laboratory, The Babraham Institute, Cambridge, CB22 3AT, United Kingdom.
Babraham Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/E/B/0000C194Wellcome Trust
6 · The paper itself

Abstract

Estrogen can modulate neuronal development and signalling by both genomic and non-genomic pathways. Many of its rapid, non-genomic effects on nervous tissue have been suggested to be mediated via the activation of the estrogen sensitive G-protein coupled receptor (GPER1 or GPR30). There has been much controversy over the cellular location, signalling properties and endogenous activators of GPER1. Here we describe the pharmacology and signalling properties of GPER1 in an immortalized embryonic hippocampal cell line, mHippoE-18. This cell line does not suffer from the inherent problems associated with the study of this receptor in native tissue or the problems associated with heterologously expression in clonal cell lines. In mHippoE-18 cells, 17β-Estradiol can mediate a dose-dependent rapid potentiation of forskolin-stimulated cyclic AMP levels but does not appear to activate the ERK1/2 pathway. The effect of 17β-Estradiol can be mimicked by the GPER1 agonist, G1, and also by tamoxifen and ICI 182,780 which activate GPER1 in a variety of other preparations. The response is not mimicked by the application of the classical estrogen receptor agonists, PPT, (an ERα agonist) or DPN, (an ERβ agonist), further suggesting that this effect of 17β-Estradiol is mediated through the activation of GPER1. However, after exposure of the cells to the GPER1 specific antagonists, G15 and G36, the stimulatory effects of the above agonists are replaced by dose-dependent inhibitions of forskolin-stimulated cyclic AMP levels. This inhibitory effect is mimicked by aldosterone in a dose-dependent way even in the absence of the GPER1 antagonists. The results are discussed in terms of possible "Biased Antagonism" whereby the antagonists change the conformation of the receptor resulting in changes in the agonist induced coupling of the receptor to different second messenger pathways.

Indexed as

Signal TransductionAdenylyl CyclasesAldosteroneAnimalsCell LineColforsinCyclic AMPEmbryo, MammalianEstradiolFulvestrantHippocampusMAP Kinase Signaling SystemMiceNitrilesPhenolsPropionates2,3-bis(4-hydroxyphenyl)-propionitrile4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenolAdenylyl CyclasesAldosteroneColforsinCyclic AMPEstradiolFulvestrantGPER1 protein, mouseNitrilesPhenolsPropionatesPyrazolesReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifen

Identifiers

PMID26998610
PMCPMC4801207
OpenAlexW2305154634

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.