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 and Pavel BABICA

Basic information

Original name

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

Authors

BRÓZMAN, Ondřej (203 Czech Republic, belonging to the institution), Jiří NOVÁK (203 Czech Republic, belonging to the institution), Alison K. BAUER (840 United States of America) and Pavel BABICA (203 Czech Republic, guarantor, belonging to the institution)

Edition

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

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30108 Toxicology

Country of publisher

Netherlands

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

URL

Impact factor

Impact factor: 4.860

RIV identification code

RIV/00216224:14310/20:00117972

Organization unit

Faculty of Science

DOI

http://dx.doi.org/10.1016/j.etap.2020.103422

UT WoS

000571540500008

Keywords in English

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

Abstract

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.

Links

EF17_043/0009632, research and development project

Name: CETOCOEN Excellence

LM2018121, research and development project

Name: Výzkumná infrastruktura RECETOX (Acronym: RECETOX RI)

Investor: Ministry of Education, Youth and Sports of the CR, RECETOX RI

Citovat

BRÓZMAN, Ondřej, Jiří NOVÁK, Alison K. BAUER and 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, vol. 79, October 2020, p. 1-12. ISSN 1382-6689. Available from: https://dx.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 = {http://dx.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 and 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, vol.~79, October 2020, p.~1-12. ISSN~1382-6689. Available from: https://dx.doi.org/10.1016/j.etap.2020.103422.

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