Evidence map›Paper›PMID 32210810›Full record

ArticleFrontiers in pharmacology2020

Connexin43 Hemichannel Targeting With TAT-Gap19 Alleviates Radiation-Induced Endothelial Cell Damage.

Raghda Ramadan, Els Vromans, Dornatien Chuo Anang, Ines Goetschalckx, Delphine Hoorelbeke, Elke Decrock, Sarah Baatout, Luc Leybaert, An Aerts

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  6. The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023
    Review
  7. Article
  8. Cx43 Hemichannel and Panx1 Channel Modulation by Gap19 andInternational journal of molecular sciences · 2023
    Article
  9. Review
  10. Article
  11. Review
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  13. Article
  14. Article
  15. Article
  16. Cardiovascular ramifications of therapy-induced endothelial cell senescence in cancer survivors.Biochimica et biophysica acta. Molecular basis of disease · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Peptidic Connexin43 Therapeutics in Cardiac Reparative Medicine.Journal of cardiovascular development and disease · 2021
    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 4 institutions in 1 country.

Raghda RamadanRadiobiology Unit, Belgian Nuclear Research Centre (SCK•CEN), Mol, Belgium.
Els VromansCentre for Environmental Health Sciences, Hasselt University, Hasselt, Belgium.
Dornatien Chuo AnangBiomedical Research Institute and Transnational University of Limburg, Hasselt University, Hasselt, Belgium.
Ines GoetschalckxProtein Chemistry, Proteomics and Epigenetic Signaling Group, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Antwerp, Belgium.
Delphine HoorelbekeDepartment of Fundamental and Basic Medical Sciences, Physiology Group, Ghent University, Ghent, Belgium.
Elke DecrockDepartment of Fundamental and Basic Medical Sciences, Physiology Group, Ghent University, Ghent, Belgium.
Sarah BaatoutRadiobiology Unit, Belgian Nuclear Research Centre (SCK•CEN), Mol, Belgium.
Luc LeybaertDepartment of Fundamental and Basic Medical Sciences, Physiology Group, Ghent University, Ghent, Belgium.
An AertsRadiobiology Unit, Belgian Nuclear Research Centre (SCK•CEN), Mol, Belgium.
Belgian Nuclear Research Centre · BEGhent University · BEHasselt University · BEUniversity of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmerging evidence indicates an excess risk of late occurring cardiovascular diseases, especially atherosclerosis, after thoracic cancer radiotherapy. Ionizing radiation (IR) induces cellular effects which may induce endothelial cell dysfunction, an early marker for atherosclerosis. In addition, intercellular communication through channels composed of transmembrane connexin proteins (Cxs), i.e. Gap junctions (direct cell-cell coupling) and hemichannels (paracrine release/uptake pathway) can modulate radiation-induced responses and therefore the atherosclerotic process. However, the role of endothelial hemichannel in IR-induced atherosclerosis has never been described before. MATERIALS AND

methodsTelomerase-immortalized human Coronary Artery/Microvascular Endothelial cells (TICAE/TIME) were exposed to X-rays (0.1 and 5 Gy). Production of reactive oxygen species (ROS), DNA damage, cell death, inflammatory responses, and senescence were assessed with or without applying a Cx43 hemichannel blocker (TAT-Gap19).

resultsWe report here that IR induces an increase in oxidative stress, cell death, inflammatory responses (IL-8, IL-1β, VCAM-1, MCP-1, and Endothelin-1) and premature cellular senescence in TICAE and TIME cells. These effects are significantly reduced in the presence of the Cx43 hemichannel-targeting peptide TAT-Gap19.

conclusionOur findings suggest that endothelial Cx43 hemichannels contribute to various IR-induced processes, such as ROS, cell death, inflammation, and senescence, resulting in an increase in endothelial cell damage, which could be protected by blocking these hemichannels. Thus, targeting Cx43 hemichannels may potentially exert radioprotective effects.

Indexed as

atherosclerosisconnexin43 hemichannelsendothelial damageionizing radiationTAT-Gap19

Identifiers

PMID32210810
PMCPMC7066501
OpenAlexW3009624749

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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.