Airborne PAHs inhibit gap junctional intercellular
communication and activate MAPKs in human bronchial epithelial
cell line

J 2020

Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line

BRÓZMAN, Ondřej; Jiří NOVÁK; Alison K. BAUER a Pavel BABICA

Základní údaje

Originální název

Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line

Autoři

BRÓZMAN, Ondřej; Jiří NOVÁK; Alison K. BAUER a Pavel BABICA

Vydání

Environmental Toxicology and Pharmacology, Amsterdam, Elsevier Science B.V. 2020, 1382-6689

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30108 Toxicology

Stát vydavatele

Nizozemské království

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 4.860

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14310/20:00117972

Organizační jednotka

Přírodovědecká fakulta

Klíčová slova anglicky

Gap junctional intercellular communication; Polycyclic aromatic hydrocarbons; Methylated anthracenes; Mitogen-activated protein kinases; Human bronchial epithelial cell line; Nongenotoxic mechanisms

Štítky

143180, rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 3. 6. 2025 20:44, Mgr. Michaela Hylsová, Ph.D.

Anotace

V originále

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 bayor 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, 1and 9methylanthracene 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.

Návaznosti

EF17_043/0009632, projekt VaV

Název: CETOCOEN Excellence

90121, velká výzkumná infrastruktura

Název: RECETOX RI

Citovat

BRÓZMAN, Ondřej; Jiří NOVÁK; Alison K. BAUER a Pavel BABICA. Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line. Environmental Toxicology and Pharmacology. Amsterdam: Elsevier Science B.V., 2020, roč. 79, October 2020, s. 1-12. ISSN 1382-6689. Dostupné z: https://doi.org/10.1016/j.etap.2020.103422.

@article{1732377,
   author = {Brózman, Ondřej and Novák, Jiří and Bauer, Alison K. and Babica, Pavel},
   article_location = {Amsterdam},
   article_number = {October 2020},
   doi = {https://doi.org/10.1016/j.etap.2020.103422},
   keywords = {Gap junctional intercellular communication; Polycyclic aromatic hydrocarbons; Methylated anthracenes; Mitogen-activated protein kinases; Human bronchial epithelial cell line; Nongenotoxic mechanisms},
   language = {eng},
   issn = {1382-6689},
   journal = {Environmental Toxicology and Pharmacology},
   note = {CZ.02.1.01/0.0/0.0/18_046/0015975 neuplatňovat.},
   title = {Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line},
   url = {https://www.sciencedirect.com/science/article/pii/S1382668920300983?via%3Dihub},
   volume = {79},
   year = {2020}
}

TY  - JOUR
ID  - 1732377
AU  - Brózman, Ondřej - Novák, Jiří - Bauer, Alison K. - Babica, Pavel
PY  - 2020
TI  - Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line
JF  - Environmental Toxicology and Pharmacology
VL  - 79
IS  - October 2020
SP  - 1-12
EP  - 1-12
PB  - Elsevier Science B.V.
SN  - 13826689
N1  - CZ.02.1.01/0.0/0.0/18_046/0015975 neuplatňovat.
KW  - Gap junctional intercellular communication
KW  - Polycyclic aromatic hydrocarbons
KW  - Methylated anthracenes
KW  - Mitogen-activated protein kinases
KW  - Human bronchial epithelial cell line
KW  - Nongenotoxic mechanisms
UR  - https://www.sciencedirect.com/science/article/pii/S1382668920300983?via%3Dihub
L2  - https://www.sciencedirect.com/science/article/pii/S1382668920300983?via%3Dihub
N2  - 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 bayor 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, 1and 9methylanthracene 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.
ER  -

BRÓZMAN, Ondřej; Jiří NOVÁK; Alison K. BAUER a Pavel BABICA. Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line. \textit{Environmental Toxicology and Pharmacology}. Amsterdam: Elsevier Science B.V., 2020, roč.~79, October 2020, s.~1-12. ISSN~1382-6689. Dostupné z: https://doi.org/10.1016/j.etap.2020.103422.

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