Evidence map›Paper›PMID 18362896›Full record

ArticleBritish journal of pharmacology2008

Endothelin (ET)-1 and ET-3 promote expression of c-fos and c-jun in human choriocarcinoma via ET(B) receptor-mediated G(i)- and G(q)-pathways and MAP kinase activation.

A Rauh, W Windischhofer, A Kovacevic, T DeVaney, E Huber, M Semlitsch, H-J Leis, W Sattler, E Malle

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2008. 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
4.1field-weighted citation impact, top 7% 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, 45 citations in OpenAlex.

  1. Trial
  2. Article
  3. Central regulation of body fluid homeostasis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2022
    Review
  4. Article
  5. Endothelin ETInternational journal of molecular sciences · 2021
    Review
  6. Article
  7. Article
  8. Epigenetic silencing of endothelin-3 in colorectal cancer.International journal of immunopathology and pharmacology · 2016
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Mechanism of cancer pain.Molecular interventions · 2010
    Review
  17. Article
  18. Article
  19. Review
  20. Regulation of the epithelial Na+ channel by endothelin-1 in rat collecting duct.American journal of physiology. Renal physiology · 2008
    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

9 authors at 1 institution in 1 country.

A RauhCenter of Molecular Medicine, Institute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
W Windischhofer
A Kovacevic
T DeVaney
E Huber
M Semlitsch
H-J Leis
W Sattler
E Malle
Medical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeEndothelins (ETs) and their G protein-coupled receptors exert key physiological functions during normal and aberrant placental development. Trophoblast cells mediate the contact between the embryo and the mother, by establishing a transient organ, the placenta. Choriocarcinoma cells display many of the biochemical and morphological characteristics of in utero invasive trophoblast cells and may therefore be used as a suitable model to study epithelial tumour progression of foetal-derived cells. EXPERIMENTAL APPROACH: The present study aimed at investigating ET receptor-mediated activation of the mitogen-activated protein kinase (MAPK) pathway in human choriocarcinoma. KEY

resultsBoth JAR and Jeg-3 choriocarcinoma cell lines expressed ET receptor subtype B (ET(B)) but not ET(A) receptor transcripts. ET(B) receptor engagement by ET-1 and ET-3 resulted in a similar time- and concentration-dependent phosphorylation of p42/44 MAPK, also known as extracellular regulated kinase 1/2. Using specific pharmacological antagonists/inhibitors, we showed that ET-1/-3-mediated signal transduction by the ET(B) receptor is transmitted via G(i)- and G(q)-dependent pathways through activation of the Src (G(i)) and protein kinase C (G(q)) axis that converge at Ras/Raf, leading to downstream activation of p42/44. On a functional level, ET(B) engagement and subsequent phosphorylation of p42/44 resulted in enhanced transcription of the immediate early response genes c-fos and c-jun, a process commonly assumed to be mediated by the ET(A) receptor, and increased cell growth and relative cell area. CONCLUSIONS AND IMPLICATIONS: As human choriocarcinoma cells secrete ETs, pharmacological antagonism of ETs and/or ET(B) receptor-mediated signal transduction could represent a likely target therapy for choriocarcinoma.

Indexed as

Blotting, WesternCell CountCell Line, TumorCell MovementChoriocarcinomaDNA PrimersEndothelin-1Endothelin-3Gene ExpressionGenes, fosGenes, junGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding Protein alpha Subunits, Gq-G11HumansMitogen-Activated Protein KinasesReceptor, Endothelin BDNA PrimersEndothelin-1Endothelin-3GTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding Protein alpha Subunits, Gq-G11Mitogen-Activated Protein KinasesReceptor, Endothelin BRNATetrazolium SaltsThiazolesthiazolyl blue

Identifiers

PMID18362896
PMCPMC2438978
OpenAlexW1982081900

What OpenQuestion holds

Textmetadata
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.