Evidence map›Paper›PMID 35749538›Full record

ArticlePloS one2022

Human endothelial cells display a rapid tensional stress increase in response to tumor necrosis factor-α.

Matthias Brandt, Volker Gerke, Timo Betz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

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  9. iScience · 2022
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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

3 authors at 1 institution in 1 country.

Matthias BrandtInstitute of Cell Biology, Center for Molecular Biology of Inflammation, University Münster, Münster, Germany.ORCID 0000-0003-1730-6228
Volker GerkeInstitute of Medical Biochemistry, Center for Molecular Biology of Inflammation, University Münster, Münster, Germany.
Timo BetzInstitute of Cell Biology, Center for Molecular Biology of Inflammation, University Münster, Münster, Germany.ORCID 0000-0002-1548-0655
University of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells form the inner layer of blood vessels, making them the first barrier between the blood and interstitial tissues; thus endothelial cells play a crucial role in inflammation. In the inflammatory response, one important element is the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α). While other pro-inflammatory agents like thrombin and histamine induce acute but transient changes in endothelial cells, which have been well studied biologically as well as mechanically, TNF-α is primarily known for its sustained effects on permeability and leukocyte recruitment. These functions are associated with transcriptional changes that take place on the timescale of hours and days. Here, we investigated the early mechanical action of TNF-α and show that even just 4 min after TNF-α was added onto human umbilical vein endothelial cell monolayers, there was a striking rise in mechanical substrate traction force and internal monolayer tension. These traction forces act primarily at the boundary of the monolayer, as was to be expected. This increased internal monolayer tension may, in addition to TNF-α's other well-studied biochemical responses, provide a mechanical signal for the cells to prepare to recruit leukocytes.

Indexed as

Endothelium, VascularTumor Necrosis Factor-alphaCells, CulturedHumansHuman Umbilical Vein Endothelial CellsThrombinThrombinTumor Necrosis Factor-alpha

Identifiers

PMID35749538
PMCPMC9232152
OpenAlexW4283447857

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.