Evidence map›Paper›PMID 23285008›Full record

ArticlePloS one2012

G-protein coupled receptor 30 (GPR30): a novel regulator of endothelial inflammation.

Subhadeep Chakrabarti, Sandra T Davidge

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 104 citations in OpenAlex.

  1. Schizophrenia gene expression profile reverted to normal levels by antipsychotics.The international journal of neuropsychopharmacology · 2014
    Trial
  2. Article
  3. GPER expression prevents estrogen-induced urinary retention in obese mice.The Journal of steroid biochemistry and molecular biology · 2024
    Article
  4. Article
  5. Review
  6. Estrogen: the forgotten player in metaflammation.Frontiers in pharmacology · 2024
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. G protein-coupled estrogen receptor 1 as a novel regulator of blood pressure.American journal of physiology. Renal physiology · 2020
    Review
  18. Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy.International journal of molecular sciences · 2020
    Review
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Subhadeep ChakrabartiDepartment of Obstetrics & Gynecology, University of Alberta, Edmonton, Alberta, Canada.
Sandra T Davidge
University of Alberta · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Estrogen, the female sex hormone, is known to exert anti-inflammatory and anti-atherogenic effects. Traditionally, estrogen effects were believed to be largely mediated through the classical estrogen receptors (ERs). However, there is increasing evidence that G-protein coupled receptor 30 (GPR30), a novel estrogen receptor, can mediate many estrogenic effects on the vasculature. Despite this, the localization and functional significance of GPR30 in the human vascular endothelium remains poorly understood. Given this background, we examined the subcellular location and potential anti-inflammatory roles of GPR30 using human umbilical vein endothelial cells as a model system. Inflammatory changes were induced by treatment with tumor necrosis factor (TNF), a pro-inflammatory cytokine involved in atherogenesis and many other inflammatory conditions. We found that GPR30 was located predominantly in the endothelial cell nuclei. Treatment with the selective GPR30 agonist G-1 partially attenuated the TNF induced upregulation of pro-inflammatory proteins such as intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). This effect was completely abolished by the selective GPR30 antagonist G-15, suggesting that it was indeed mediated in a GPR30 dependent manner. Interestingly, estrogen alone had no effects on TNF-treated endothelium. Concomitant activation of the classical ERs blocked the anti-inflammatory effects of G-1, indicating opposing effects of GPR30 and the classical ERs. Our findings demonstrate that endothelial GPR30 is a novel regulator of the inflammatory response which could be a potential therapeutic target against atherosclerosis and other inflammatory diseases.

Indexed as

Anti-Inflammatory AgentsCell NucleusCyclopentanesEndothelium, VascularEstradiolHumansHuman Umbilical Vein Endothelial CellsInflammationIntercellular Adhesion Molecule-1NF-kappa BQuinolinesReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifenTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-11-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanoneafimoxifeneAnti-Inflammatory AgentsCyclopentanesEstradiolGPER1 protein, humanIntercellular Adhesion Molecule-1NF-kappa BQuinolinesReceptors, EstrogenReceptors, G-Protein-CoupledTamoxifenTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID23285008
PMCPMC3527521
OpenAlexW1971671660

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.