Show simple item record

dc.contributor.authorSekine, Takashi
dc.contributor.authorHirata, Tadashi
dc.contributor.authorIshikawa, Shinkichi
dc.contributor.authorIto, Shigeaki
dc.contributor.authorIshimori, Kanae
dc.contributor.authorMatsumura, Kazushi
dc.contributor.authorMuraki, Katsuhiko
dc.date.accessioned2019-09-24T23:47:53Z
dc.date.available2019-09-24T23:47:53Z
dc.date.issued2019
dc.identifier.issn0260-437X
dc.identifier.doi10.1002/jat.3761
dc.identifier.urihttp://hdl.handle.net/10072/387710
dc.description.abstractCigarette smoke (CS) is a complex mixture of chemicals and interacts with various physiological processes. We previously reported that nuclear factor erythroid 2-related factor 2 (NRF2) was the most sensitive transcription factor to aqueous CS extract (AqCSE) exposure in monolayer cultured human bronchial epithelial cell lines. Recently, in vitro three-dimensional (3D) culture models have been used to supplement pharmacological and toxicological assessments. Bronchial epithelium models in particular are useful for the evaluation of substances that directly contact the respiratory tract, such as CS. In the present study, we used 3D-cultured human bronchial epithelial cells (HBECs) to assess activation of transcription factors and relevant gene expression in response to AqCSE, primarily focusing on NRF2 and nuclear factor-kappa B (NF-κB) pathways. The 3D-cultured HBECs exposed to AqCSE showed expression of NRF2 and its nuclear translocation in addition to upregulation of genes related to oxidative stress. Our results suggest that the NRF2 pathway was the dominant pathway when 3D-cultured HBECs were exposed to AqCSE at a low dose, supporting our previous findings that NRF2 was the most sensitive transcription factor in response to AqCSE. Expression and nuclear translocation of NF-κB were not increased, although proinflammatory genes were upregulated. However, another inflammation-related transcription factor, activation protein 1, was induced by AqCSE. Gene classification analysis suggested that induction of the inflammatory response by AqCSE was dependent on NRF2 and activation protein 1 rather than NF-κB.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherWiley
dc.publisher.placeUnited Kingdom
dc.relation.ispartofpagefrom717
dc.relation.ispartofpageto725
dc.relation.ispartofissue5
dc.relation.ispartofjournalJournal of Applied Toxicology
dc.relation.ispartofvolume39
dc.subject.fieldofresearchPharmacology and pharmaceutical sciences
dc.subject.fieldofresearchcode3214
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsToxicology
dc.subject.keywordscigarette smoke
dc.subject.keywordsthree-dimensional culture
dc.titleRegulation of NRF2, AP-1 and NF-kappa B by cigarette smoke exposure in three-dimensional human bronchial epithelial cells
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationSekine, T; Hirata, T; Ishikawa, S; Ito, S; Ishimori, K; Matsumura, K; Muraki, K, Regulation of NRF2, AP-1 and NF-kappa B by cigarette smoke exposure in three-dimensional human bronchial epithelial cells, Journal of Applied Toxicology, 2019, 39 (5), pp. 717-725
dcterms.dateAccepted2018-11-08
dc.date.updated2019-09-24T05:07:49Z
gro.hasfulltextNo Full Text
gro.griffith.authorMuraki, Katsuhiko


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record