Epidermal growth factor receptor (EGFR) and neuregulin (Neu) activation in human airway epithelial cells exposed to nickel acetate

Giunta, S; Castorina, A; Scuderi, S; Patti, C; D'Agata, V

Epidermal growth factor receptor (EGFR) and neuregulin (Neu) activation in human airway epithelial cells exposed to nickel acetate

Giunta, S Castorina, A

Scuderi, S Patti, C D'Agata, V

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Publication Type:: Journal Article
Citation:: Toxicology in Vitro, 2012, 26 (2), pp. 280 - 287
Issue Date:: 2012-03-01

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Field	Value	Language
dc.contributor.author	Giunta, S	en_US
dc.contributor.author	Castorina, A https://orcid.org/0000-0001-7037-759X	en_US
dc.contributor.author	Scuderi, S	en_US
dc.contributor.author	Patti, C	en_US
dc.contributor.author	D'Agata, V	en_US
dc.date.available	2011-12-13	en_US
dc.date.issued	2012-03-01	en_US
dc.identifier.citation	Toxicology in Vitro, 2012, 26 (2), pp. 280 - 287	en_US
dc.identifier.issn	0887-2333	en_US
dc.identifier.uri	http://hdl.handle.net/10453/115243
dc.description.abstract	Nickel compounds are potential carcinogenic agents that produce a range of biological effects, including inhibition of cell death. Because suppression of apoptosis is thought to contribute to the initiation of carcinogenesis, we investigated the effects of nickel acetate (Ni 2+) treatment on apoptosis in two different airway epithelial cell lines (A549 and Beas-2B, respectively). Furthermore, since both the epidermal growth factor receptor (EGFR) and neuregulin (Neu) are involved in neoplastic development, mRNAs and expression levels of total and phosphorylated proteins (p-EGFR Tyr1173 and p-Neu Tyr1248, respectively) were also measured. We found that exposure of A549 cells to Ni 2+ resulted in significantly reduced cell viability, as well as increased apoptosis and DNA fragmentation at relatively low concentrations (0.1 and 0.5mM) after 24 and 48h. These changes were accompanied by reduced EGFR and Neu mRNAs and proteins, phosphorylated proteins as well as decreased Bcl-2 and increased BAX protein expression. Conversely, Beas-2B cells exposed to equivalent concentrations of Ni 2+ did not show evident signs of apoptosis and DNA damage, hence showing increased expression and phosphorylation of both EGFR and Neu, increased Bcl-2 and reduced BAX expression. Altogether, our finding indicate that Ni 2+ exposure differently affects apoptosis initiation either in non-tumorigenic (Beas-2B) and tumorigenic airway epithelial cells (A549), suggesting a potential involvement of EGFR/Neu receptors. © 2011 Elsevier Ltd.	en_US
dc.relation.ispartof	Toxicology in Vitro	en_US
dc.relation.isbasedon	10.1016/j.tiv.2011.12.012	en_US
dc.subject.classification	Toxicology	en_US
dc.subject.mesh	Bronchi	en_US
dc.subject.mesh	Pulmonary Alveoli	en_US
dc.subject.mesh	Cell Line	en_US
dc.subject.mesh	Cell Line, Tumor	en_US
dc.subject.mesh	Epithelial Cells	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	DNA Damage	en_US
dc.subject.mesh	Acetates	en_US
dc.subject.mesh	Organometallic Compounds	en_US
dc.subject.mesh	Receptor, Epidermal Growth Factor	en_US
dc.subject.mesh	Neuregulins	en_US
dc.subject.mesh	Proto-Oncogene Proteins c-bcl-2	en_US
dc.subject.mesh	RNA, Messenger	en_US
dc.subject.mesh	Air Pollutants, Occupational	en_US
dc.subject.mesh	Apoptosis	en_US
dc.subject.mesh	Cell Survival	en_US
dc.subject.mesh	bcl-2-Associated X Protein	en_US
dc.subject.mesh	ErbB Receptors	en_US
dc.title	Epidermal growth factor receptor (EGFR) and neuregulin (Neu) activation in human airway epithelial cells exposed to nickel acetate	en_US
dc.type	Journal Article
utslib.citation.volume	2	en_US
utslib.citation.volume	26	en_US
utslib.for	1115 Pharmacology and Pharmaceutical Sciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	open_access
pubs.issue	2	en_US
pubs.publication-status	Published	en_US
pubs.volume	26	en_US

Abstract:

Nickel compounds are potential carcinogenic agents that produce a range of biological effects, including inhibition of cell death. Because suppression of apoptosis is thought to contribute to the initiation of carcinogenesis, we investigated the effects of nickel acetate (Ni 2+) treatment on apoptosis in two different airway epithelial cell lines (A549 and Beas-2B, respectively). Furthermore, since both the epidermal growth factor receptor (EGFR) and neuregulin (Neu) are involved in neoplastic development, mRNAs and expression levels of total and phosphorylated proteins (p-EGFR Tyr1173 and p-Neu Tyr1248, respectively) were also measured. We found that exposure of A549 cells to Ni 2+ resulted in significantly reduced cell viability, as well as increased apoptosis and DNA fragmentation at relatively low concentrations (0.1 and 0.5mM) after 24 and 48h. These changes were accompanied by reduced EGFR and Neu mRNAs and proteins, phosphorylated proteins as well as decreased Bcl-2 and increased BAX protein expression. Conversely, Beas-2B cells exposed to equivalent concentrations of Ni 2+ did not show evident signs of apoptosis and DNA damage, hence showing increased expression and phosphorylation of both EGFR and Neu, increased Bcl-2 and reduced BAX expression. Altogether, our finding indicate that Ni 2+ exposure differently affects apoptosis initiation either in non-tumorigenic (Beas-2B) and tumorigenic airway epithelial cells (A549), suggesting a potential involvement of EGFR/Neu receptors. © 2011 Elsevier Ltd.

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http://hdl.handle.net/10453/115243