Evidence map›Paper›PMID 30273401›Full record

ArticlePloS one2018

Inflammatory cytokine oncostatin M induces endothelial activation in macro- and microvascular endothelial cells and in APOE*3Leiden.CETP mice.

Danielle van Keulen, Marianne G Pouwer, Gerard Pasterkamp, Alain J van Gool, Maarten D Sollewijn Gelpke, Hans M G Princen, Dennie Tempel

Abstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Trial
  2. Distinct Blood and Lung Proteins Drive Pulmonary Capillary Leak in Children With Severe Hypoxemic Respiratory Failure.Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2026
    Observational
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  4. Article
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  7. Article
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  10. Article
  11. Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Common Variants Associated WithFrontiers in cardiovascular medicine · 2021
    Article
  18. Article
  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

7 authors.

Danielle van KeulenLaboratory of Experimental Cardiology, University Medical Centre Utrecht, Utrecht, The Netherlands.
Marianne G PouwerTNO-Metabolic Health Research, Gaubius Laboratory, Leiden, The Netherlands.ORCID 0000-0001-9657-871X
Gerard PasterkampLaboratory of Experimental Cardiology, University Medical Centre Utrecht, Utrecht, The Netherlands.
Alain J van GoolTNO- Microbiology & Systems Biology, Zeist, The Netherlands.ORCID 0000-0003-0010-5286
Maarten D Sollewijn GelpkeMolecular Profiling Consulting, London, England.
Hans M G PrincenTNO-Metabolic Health Research, Gaubius Laboratory, Leiden, The Netherlands.ORCID 0000-0002-7206-1596
Dennie TempelLaboratory of Experimental Cardiology, University Medical Centre Utrecht, Utrecht, The Netherlands.ORCID 0000-0002-8061-6483

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsEndothelial activation is involved in many chronic inflammatory diseases, such as atherosclerosis, and is often initiated by cytokines. Oncostatin M (OSM) is a relatively unknown cytokine that has been suggested to play a role in both endothelial activation and atherosclerosis. We comprehensively investigated the effect of OSM on endothelial cell activation from different vascular beds and in APOE*3Leiden.CETP mice. METHODS AND

resultsHuman umbilical vein endothelial cells, human aortic endothelial cells and human microvascular endothelial cells cultured in the presence of OSM express elevated MCP-1, IL-6 and ICAM-1 mRNA levels. Human umbilical vein endothelial cells and human aortic endothelial cells additionally expressed increased VCAM-1 and E-selectin mRNA levels. Moreover, ICAM-1 membrane expression is increased as well as MCP-1, IL-6 and E-selectin protein release. A marked increase was observed in STAT1 and STAT3 phosphorylation indicating that the JAK/STAT pathway is involved in OSM signaling. OSM signals through the LIF receptor alfa (LIFR) and the OSM receptor (OSMR). siRNA knockdown of the LIFR and the OSMR revealed that simultaneous knockdown is necessary to significantly reduce MCP-1 and IL-6 secretion, VCAM-1 and E-selectin shedding and STAT1 and STAT3 phosphorylation after OSM stimulation. Moreover, OSM administration to APOE*3Leiden.CETP mice enhances plasma E-selectin levels and increases ICAM-1 expression and monocyte adhesion in the aortic root area. Furthermore, Il-6 mRNA expression was elevated in the aorta of OSM treated mice.

conclusionOSM induces endothelial activation in vitro in endothelial cells from different vascular beds through activation of the JAK/STAT cascade and in vivo in APOE*3Leiden.CETP mice. Since endothelial activation is an initial step in atherosclerosis development, OSM may play a role in the initiation of atherosclerotic lesion formation.

Indexed as

Signal TransductionAnimalsCell AdhesionCells, CulturedChemokine CCL2Cholesterol Ester Transfer ProteinsEndothelial CellsE-SelectinHumansHuman Umbilical Vein Endothelial CellsIntercellular Adhesion Molecule-1Interleukin-6MiceOncostatin MSTAT Transcription FactorsChemokine CCL2Cholesterol Ester Transfer ProteinsE-SelectinIntercellular Adhesion Molecule-1Interleukin-6Oncostatin MSTAT Transcription Factors

Identifiers

PMID30273401
PMCPMC6166945

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Registered trials

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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.