Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články
Grantová podpora
R15 ES024893
NIEHS NIH HHS - United States
PubMed
32492535
PubMed Central
PMC7486243
DOI
10.1016/j.etap.2020.103422
PII: S1382-6689(20)30098-3
Knihovny.cz E-zdroje
- Klíčová slova
- Gap junctional intercellular communication, Human bronchial epithelial cell line, Methylated anthracenes, Mitogen-activated protein kinases, Nongenotoxic mechanisms, Polycyclic aromatic hydrocarbons,
- MeSH
- bronchy cytologie MeSH
- buněčné linie MeSH
- epitelové buňky účinky léků fyziologie MeSH
- lidé MeSH
- mezerový spoj účinky léků MeSH
- mezibuněčná komunikace účinky léků MeSH
- mitogenem aktivované proteinkinasy metabolismus MeSH
- polycyklické aromatické uhlovodíky toxicita MeSH
- viabilita buněk účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- mitogenem aktivované proteinkinasy MeSH
- polycyklické aromatické uhlovodíky MeSH
Inhalation exposures to polycyclic aromatic hydrocarbons (PAHs) have been associated with various adverse health effects, including chronic lung diseases and cancer. Using human bronchial epithelial cell line HBE1, we investigated the effects of structurally different PAHs on tissue homeostatic processes, namely gap junctional intercellular communication (GJIC) and MAPKs activity. Rapid (<1 h) and sustained (up to 24 h) inhibition of GJIC was induced by low/middle molecular weight (MW) PAHs, particularly by those with a bay- or bay-like region (1- and 9-methylanthracene, fluoranthene), but also by fluorene and pyrene. In contrast, linear low MW (anthracene, 2-methylanthracene) or higher MW (chrysene) PAHs did not affect GJIC. Fluoranthene, 1- and 9-methylanthracene induced strong and sustained activation of MAPK ERK1/2, whereas MAPK p38 was activated rather nonspecifically by all tested PAHs. Low/middle MW PAHs can disrupt tissue homeostasis in human airway epithelium via structure-dependent nongenotoxic mechanisms, which can contribute to their human health hazards.
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