Evidence map›Paper›PMID 23437087›Full record

ArticlePloS one2013

Overexpression of endoglin modulates TGF-β1-signalling pathways in a novel immortalized mouse hepatic stellate cell line.

Steffen K Meurer, Muhammad Alsamman, Hacer Sahin, Hermann E Wasmuth, Tatiana Kisseleva, David A Brenner, Christian Trautwein, Ralf Weiskirchen, David Scholten

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Working with Immortalized Hepatic Stellate Cell Lines.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  16. Molecular and cellular mechanisms of liver fibrosis and its regression.Nature reviews. Gastroenterology & hepatology · 2021
    Review
  17. Article
  18. Article
  19. Article
  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

9 authors at 3 institutions in 2 countries.

Steffen K MeurerInstitute of Clinical Chemistry and Pathobiochemistry, RWTH University Hospital Aachen, Aachen, Germany.
Muhammad Alsamman
Hacer Sahin
Hermann E Wasmuth
Tatiana Kisseleva
David A Brenner
Christian Trautwein
Ralf Weiskirchen
David Scholten
Universitätsklinikum Aachen · DERWTH Aachen University · DEUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic stellate cells (HSCs) play a major role in the pathogenesis of liver fibrosis. Working on primary HSCs requires difficult isolation procedures; therefore we have generated and here characterize a mouse hepatic stellate cell line expressing GFP under control of the collagen 1(I) promoter/enhancer. These cells are responsive to pro-fibrogenic stimuIi, such as PDGF or TGF-β1, and are able to activate intracellular signalling pathways including Smads and MAP kinases. Nevertheless, due to the basal level of activation, TGF-β1 did not significantly induce GFP expression contrasting the TGF-β1 regulated endogenous collagen I expression. We could demonstrate that the accessory TGF-β-receptor endoglin, which is endogenously expressed at very low levels, has a differential effect on signalling of these cells when transiently overexpressed. In the presence of endoglin activation of Smad1/5/8 was drastically enhanced. Moreover, the phosphorylation of ERK1/2 was increased, and the expression of vimentin, α-smooth muscle actin and connective tissue growth factor was upregulated. Endoglin induced a slight increase in expression of the inhibitor of differentiation-2 while the amount of endogenous collagen type I was reduced. Therefore, this profibrogenic cell line with hepatic stellate cell origin is not only a promising novel experimental tool, which can be used in vivo for cell tracing experiments. Furthermore it allows investigating the impact of various regulatory proteins (e.g. endoglin) on profibrogenic signal transduction, differentiation and hepatic stellate cell biology.

Indexed as

Signal TransductionAnimalsBecaplerminBiomarkersCell Line, TransformedCollagenEndoglinEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFluorescenceGreen Fluorescent ProteinsHepatic Stellate CellsIntracellular Signaling Peptides and ProteinsLigandsLiver CirrhosisMiceBecaplerminBiomarkersCollagenEndoglinEng protein, mouseExtracellular Signal-Regulated MAP KinasesGreen Fluorescent ProteinsIntracellular Signaling Peptides and ProteinsLigandsProto-Oncogene Proteins c-sisTransforming Growth Factor beta1

Identifiers

PMID23437087
PMCPMC3577806
OpenAlexW2099682100

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.