Evidence map›Paper›PMID 33114474›Full record

ArticleProteomes2020

Radiation Response of Human Cardiac Endothelial Cells Reveals a Central Role of the cGAS-STING Pathway in the Development of Inflammation.

Jos Philipp, Ronan Le Gleut, Christine von Toerne, Prabal Subedi, Omid Azimzadeh, Michael J Atkinson, Soile Tapio

Open access · goldAbstract read
In one paragraph

Article in Proteomes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

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  15. Cytosolic DNA sensing by cGAS: regulation, function, and human diseases.Signal transduction and targeted therapy · 2021
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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

7 authors at 1 institution in 1 country.

Jos PhilippInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health GmbH, 85764 Neuherberg, Germany.
Ronan Le GleutInstitute of Computational Biology, Helmholtz Center Munich, German Research Center for Environmental Health GmbH, 85764 Neuherberg, Germany.
Christine von ToerneResearch Unit Protein Science, Helmholtz Center Munich, German Research Center for Environmental Health GmbH, 85764 Neuherberg, Germany.
Prabal SubediInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health GmbH, 85764 Neuherberg, Germany.ORCID 0000-0002-5661-3776
Omid AzimzadehInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health GmbH, 85764 Neuherberg, Germany.ORCID 0000-0001-8984-0388
Michael J AtkinsonInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health GmbH, 85764 Neuherberg, Germany.
Soile TapioInstitute of Radiation Biology, Helmholtz Center Munich, German Research Center for Environmental Health GmbH, 85764 Neuherberg, Germany.ORCID 0000-0001-9860-3683
Helmholtz Zentrum München · DE

Funding

Federal Ministry of Education and Research of Germany (BMBF) 02NUK038B
6 · The paper itself

Abstract

Radiation-induced inflammation leading to the permeability of the endothelial barrier may increase the risk of cardiovascular disease. The aim of this study was to investigate potential mechanisms in vitro at the level of the proteome in human coronary artery endothelial cells (HCECest2) that were exposed to radiation doses of 0, 0.25, 0.5, 2.0 and 10 Gy (60Co-γ). Proteomics analysis was performed using mass spectrometry in a label-free data-independent acquisition mode. The data were validated using bioinformatics and immunoblotting. The low- and moderate-dose-irradiated samples (0.25 Gy, 0.5 Gy) showed only scarce proteome changes. In contrast, an activation of DNA-damage repair, inflammation, and oxidative stress pathways was seen after the high-dose treatments (2 and 10 Gy). The level of the DNA damage response protein DDB2 was enhanced early at the 10 Gy dose. The expression of proteins belonging to the inflammatory response or cGAS-STING pathway (STING, STAT1, ICAM1, ISG15) increased in a dose-dependent manner, showing the strongest effects at 10 Gy after one week. This study suggests a connection between the radiation-induced DNA damage and the induction of inflammation which supports the inhibition of the cGAS-STING pathway in the prevention of radiation-induced cardiovascular disease.

Indexed as

cGAS-STING-pathwaydata-independent acquisitionDDB2endothelial cellsinflammationionizing radiationproteomicsSTAT1

Identifiers

PMID33114474
PMCPMC7709117
OpenAlexW3093637571

What OpenQuestion holds

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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.