File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Gene Expression Profile And Toxic Effects In Human Bronchial Epithelial Cells Exposed To Zearalenone

TitleGene Expression Profile And Toxic Effects In Human Bronchial Epithelial Cells Exposed To Zearalenone
Authors
Issue Date2014
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2014, v. 9 n. 5, article no. e96404 How to Cite?
AbstractZearalenone (ZEA), a mycoestrogen produced by Fusarium fungal species, is mainly found in cereal crops such as maize, wheat and barley. Although ZEA has been reported to be present in air, little is known about the health risk or the molecular basis of action when lung cells are exposed to ZEA. As ZEA has a similar structure to estrogen, its potential risk as an endocrine disrupting chemical (EDC) has thus aroused both environmental and public health concerns. The purpose of this study is to identify the responses and underlying molecular changes that occur when human bronchial epithelial BEAS-2B cells are exposed to ZEA. Differential gene expression profiles were identified in cells that were treated with 40 µM ZEA for 6 h and 24 h by high-throughput microarray analysis using Affymetrix Human Gene 2.0 GeneChip. The array results showed that after ZEA treatment, 262 genes at 6 h and 1073 genes at 24 h were invovled in the differential regulation. Pathway analysis revealed that diverse cellular processes were affected when lung cells were exposed to ZEA resulting in impaired response to DNA damage, cell cycle arrest, down-regulation of inflammatory responses and alterations of epigenetic marks. Results of further experiments indicated that 40 µM ZEA decreased cell viability, induced apoptosis and promoted reactive oxygen species (ROS) generation in a time-dependent manner. Immuno-suppressive effects of ZEA were further revealed through the suppression of lipopolysaccharide (LPS)-induced expression of pro-inflammatory cytokines (IL-6, IL-8 and IL-1β). Interestingly, the level of global DNA methylation was markedly decreased after 24 h exposure to ZEA. Collectively, these observations suggested that a broad range of toxic effects are elicited by ZEA. Particularly, ROS may play a pivotal role in ZEA-induced cell death. These adverse effects observed in lung cells suggest that exposure to ZEA may increase susceptibility of lung cells to diseases and required further investigations.April 5, 2014
Persistent Identifierhttp://hdl.handle.net/10722/201542
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorSo, MYen_US
dc.contributor.authorTian, ZPen_US
dc.contributor.authorPhoon, YSen_US
dc.contributor.authorSha, Sen_US
dc.contributor.authorAntoniou, MNen_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorWu, RSSen_US
dc.contributor.authorTan-Un, KCen_US
dc.date.accessioned2014-08-21T07:30:23Z-
dc.date.available2014-08-21T07:30:23Z-
dc.date.issued2014en_US
dc.identifier.citationPlos One, 2014, v. 9 n. 5, article no. e96404en_US
dc.identifier.issn1932-6203-
dc.identifier.urihttp://hdl.handle.net/10722/201542-
dc.description.abstractZearalenone (ZEA), a mycoestrogen produced by Fusarium fungal species, is mainly found in cereal crops such as maize, wheat and barley. Although ZEA has been reported to be present in air, little is known about the health risk or the molecular basis of action when lung cells are exposed to ZEA. As ZEA has a similar structure to estrogen, its potential risk as an endocrine disrupting chemical (EDC) has thus aroused both environmental and public health concerns. The purpose of this study is to identify the responses and underlying molecular changes that occur when human bronchial epithelial BEAS-2B cells are exposed to ZEA. Differential gene expression profiles were identified in cells that were treated with 40 µM ZEA for 6 h and 24 h by high-throughput microarray analysis using Affymetrix Human Gene 2.0 GeneChip. The array results showed that after ZEA treatment, 262 genes at 6 h and 1073 genes at 24 h were invovled in the differential regulation. Pathway analysis revealed that diverse cellular processes were affected when lung cells were exposed to ZEA resulting in impaired response to DNA damage, cell cycle arrest, down-regulation of inflammatory responses and alterations of epigenetic marks. Results of further experiments indicated that 40 µM ZEA decreased cell viability, induced apoptosis and promoted reactive oxygen species (ROS) generation in a time-dependent manner. Immuno-suppressive effects of ZEA were further revealed through the suppression of lipopolysaccharide (LPS)-induced expression of pro-inflammatory cytokines (IL-6, IL-8 and IL-1β). Interestingly, the level of global DNA methylation was markedly decreased after 24 h exposure to ZEA. Collectively, these observations suggested that a broad range of toxic effects are elicited by ZEA. Particularly, ROS may play a pivotal role in ZEA-induced cell death. These adverse effects observed in lung cells suggest that exposure to ZEA may increase susceptibility of lung cells to diseases and required further investigations.April 5, 2014en_US
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action-
dc.relation.ispartofPlos Oneen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleGene Expression Profile And Toxic Effects In Human Bronchial Epithelial Cells Exposed To Zearalenoneen_US
dc.typeArticleen_US
dc.identifier.emailZhang, J: jzhang1@hku.hken_US
dc.identifier.emailWu, RSS: rudolfwu@hku.hken_US
dc.identifier.emailTan-Un, KC: kctanun@hkucc.hku.hken_US
dc.identifier.authorityZhang, J=rp01713en_US
dc.identifier.authorityWu, RSS=rp01398en_US
dc.identifier.authorityTan-Un, KC=rp00787en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0096404-
dc.identifier.pmid24788721-
dc.identifier.pmcidPMC4008614-
dc.identifier.hkuros232212en_US
dc.identifier.volume9-
dc.identifier.issue5en_US
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats