Evidence map›Paper›PMID 26867691›Full record

ArticleScientific reports2016

WISP1 mediates IL-6-dependent proliferation in primary human lung fibroblasts.

S Klee, M Lehmann, D E Wagner, H A Baarsma, M Königshoff

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.6field-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

37 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. An overview of CCN4 (WISP1) role in human diseases.Journal of translational medicine · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Optimal CCN4 Immunofluorescence for Tissue Microarray.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. WNT Signalling in Lung Physiology and Pathology.Handbook of experimental pharmacology · 2021
    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

5 authors at 2 institutions in 1 country.

S KleeComprehensive Pneumology Center, Helmholtz Zentrum München, Munich, Germany.
M LehmannComprehensive Pneumology Center, Helmholtz Zentrum München, Munich, Germany.
D E WagnerComprehensive Pneumology Center, Helmholtz Zentrum München, Munich, Germany.
H A BaarsmaComprehensive Pneumology Center, Helmholtz Zentrum München, Munich, Germany.
M KönigshoffComprehensive Pneumology Center, Helmholtz Zentrum München, Munich, Germany.
Helmholtz Zentrum München · DEGerman Center for Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease. IPF is characterized by epithelial cell injury and reprogramming, increases in (myo)fibroblasts, and altered deposition of extracellular matrix. The Wnt1-inducible signaling protein 1 (WISP1) is involved in impaired epithelial-mesenchymal crosstalk in pulmonary fibrosis. Here, we aimed to further investigate WISP1 regulation and function in primary human lung fibroblasts (phLFs). We demonstrate that WISP1 is directly upregulated by Transforming growth factor β1 (TGFβ1) and Tumor necrosis factor α (TNFα) in phLFs, using a luciferase-based reporter system. WISP1 mRNA and protein secretion increased in a time- and concentration-dependent manner by TGFβ1 and TNFα in phLFs, as analysed by qPCR and ELISA, respectively. Notably, WISP1 is required for TGFβ1- and TNFα-dependent induction of interleukin 6 (IL-6), a mechanism that is conserved in IPF phLFs. The siRNA-mediated WISP1 knockdown led to a significant IL-6 reduction after TGFβ1 or TNFα stimulation. Furthermore, siRNA-mediated downregulation or antibody-mediated neutralization of WISP1 reduced phLFs proliferation, a process that was in part rescued by IL-6. Taken together, these results strongly indicate that WISP1-induced IL-6 expression contributes to the pro-proliferative effect on fibroblasts, which is likely orchestrated by a variety of profibrotic mediators, including Wnts, TGFβ1 and TNFα.

Indexed as

CCN Intercellular Signaling ProteinsCell ProliferationCells, CulturedFibroblastsHumansInterleukin-6LungModels, BiologicalPromoter Regions, GeneticProto-Oncogene ProteinsPulmonary FibrosisSignal TransductionTransforming Growth Factor beta1Tumor Necrosis Factor-alphaCCN4 protein, humanCCN Intercellular Signaling ProteinsIL6 protein, humanInterleukin-6Proto-Oncogene ProteinsTransforming Growth Factor beta1Tumor Necrosis Factor-alpha

Identifiers

PMID26867691
PMCPMC4751539
OpenAlexW2395692822

What OpenQuestion holds

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LicenceCC BY
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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.