ArticleScientific reports2017
Benzo(a)pyrene triggers desensitization of β2-adrenergic pathway.
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.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Mechanisms and Manifestations of Ligand Bias in Signaling: Focus on Receptor Tyrosine Kinases.Chemical reviews · 2026Review
- PM2.5 toxin benzo[a]pyrene induces life-limiting inflammation and oxidative stress in the airway by up-regulation of TRPC6 and inactivation of β2AR/CFTR signaling.bioRxiv : the preprint server for biology · 2026Article
- The Effects of Air Pollution on Neurological Diseases: A Narrative Review on Causes and Mechanisms.Toxics · 2025Review
- Epigenetics of Chronic Stress: Mechanisms and Health Impacts.Current genomics · 2025Review
- Benzo[a]pyrene disrupts LH/hCG-dependent mouse Leydig cell steroidogenesis through receptor/Gαs protein targeting.Scientific reports · 2024Article
- The βFrontiers in immunology · 2024Article
- Effects of organic chemicals from diesel exhaust particles on adipocytes differentiated from human mesenchymal stem cells.Basic & clinical pharmacology & toxicology · 2023Article
- Potential role of polycyclic aromatic hydrocarbons in air pollution-induced non-malignant respiratory diseases.Respiratory research · 2020Review
- Potential role of polycyclic aromatic hydrocarbons as mediators of cardiovascular effects from combustion particles.Environmental health : a global access science source · 2019Review
- Genome-Wide Transcriptional and Functional Analysis of Human T Lymphocytes Treated with Benzo[International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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