Evidence map›Paper›PMID 28607424›Full record

ArticleScientific reports2017

Benzo(a)pyrene triggers desensitization of β2-adrenergic pathway.

Abdullah Mayati, Normand Podechard, Manuelle Rineau, Lydie Sparfel, Dominique Lagadic-Gossmann, Olivier Fardel, Eric Le Ferrec

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. 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
1.0field-weighted citation impact, top 25% 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, 19 citations in OpenAlex.

  1. Review
  2. Article
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  5. Article
  6. The βFrontiers in immunology · 2024
    Article
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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 3 institutions in 1 country.

Abdullah MayatiInserm U1085, Institut de Recherche en Santé, Environnement, Travail, Rennes, France.
Normand PodechardInserm U1085, Institut de Recherche en Santé, Environnement, Travail, Rennes, France.
Manuelle RineauInserm U1085, Institut de Recherche en Santé, Environnement, Travail, Rennes, France.
Lydie SparfelInserm U1085, Institut de Recherche en Santé, Environnement, Travail, Rennes, France.
Dominique Lagadic-GossmannInserm U1085, Institut de Recherche en Santé, Environnement, Travail, Rennes, France.
Olivier FardelInserm U1085, Institut de Recherche en Santé, Environnement, Travail, Rennes, France.
Eric Le FerrecInserm U1085, Institut de Recherche en Santé, Environnement, Travail, Rennes, France. eric.leferrec@univ-rennes1.fr.
Institut de Recherche en Santé, Environnement et Travail · FRInstitut des Sciences Chimiques de Rennes · FRUniversité de Rennes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to environmental polycyclic aromatic hydrocarbons (PAHs), such as benzo(a)pyrene (B(a)P), has been linked to several health-threatening risks. PAHs were also shown to hinder adrenergic receptor (ADR) responses. As we previously demonstrated that B(a)P can directly interact with the β2ADR, we investigated here whether B(a)P could decrease β2ADR responsiveness by triggering receptor desensitization phenomena. We firstly showed that exposure to B(a)P reduced β2ADR-mediated epinephrine-induced induction of NR4A gene mRNAs and of intracellular cAMP. Analysis of β2ADR protein expression demonstrated that B(a)P rapidly decreased membrane expression of β2ADR with a subsequent degradation of receptor protein. B(a)P exposure concomitantly rapidly increased the β2ADR mRNA levels. The use of the β-blockers, propranolol and ICI 118.551, demonstrated the involvement of β2ADR itself in this increase. However, sustained exposure to B(a)P induced a diminution of β2ADR mRNA steady-state as a result of the acceleration of its degradation. Together, these results show that, beside the well-known activation of the aryl hydrocarbon receptor, PAH deleterious effects may involve the dysfunction of adrenergic responses through, in part, the desensitization of β2ADR. This may be taken in consideration when β2-agonists/antagonists are administered in patients exposed to important concentrations of PAHs, e.g. in cigarette smokers.

Indexed as

Adrenergic beta-AgonistsBenzo(a)pyreneCell MembraneCyclic AMPEndothelial CellsEpinephrineGene Expression RegulationHumansNuclear Receptor Subfamily 4, Group A, Member 1ProteolysisReceptors, Adrenergic, beta-2RNA, MessengerRNA StabilitySignal TransductionAdrenergic beta-AgonistsBenzo(a)pyreneCyclic AMPEpinephrineNuclear Receptor Subfamily 4, Group A, Member 1Receptors, Adrenergic, beta-2RNA, Messenger

Identifiers

PMID28607424
PMCPMC5468268
OpenAlexW2621475890

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.