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タイトル: | Cigarette smoke reversibly activates hypoxia-inducible factor 1 in a reactive oxygen species-dependent manner |
著者: | Daijo, Hiroki Hoshino, Yuma Kai, Shinichi Suzuki, Kengo Nishi, Kenichiro Matsuo, Yoshiyuki Harada, Hiroshi https://orcid.org/0000-0001-7507-3173 (unconfirmed) Hirota, Kiichi |
著者名の別形: | 大条, 紘樹 原田, 浩 |
発行日: | 29-Sep-2016 |
出版者: | Springer Nature |
誌名: | Scientific Reports |
巻: | 6 |
論文番号: | 34424 |
抄録: | Cigarette smoke (CS) is a major contributor to the development of a large number of fatal and debilitating disorders. However, the precise molecular mechanisms underlying the effects of CS in lung disease are largely unknown. To elucidate these pathophysiological processes, we examined the in vitro and in vivo effects of CS extract (CSE) and CS on the transcription factor, hypoxia-inducible factor 1 (HIF-1). CSE induced concentration- and time-dependent accumulation of HIF-1α protein in human lung epithelial-like cells under non-hypoxic conditions. Genes upregulated by HIF-1, including vascular endothelial growth factor and regulated in development and DNA damage response 1, both of which are involved in smoking-induced emphysematous changes, were increased by CSE treatment under non-hypoxic conditions in vitro and in vivo. Further investigation revealed that reactive oxygen species were generated in cells exposed to CSE and were required for CSE-mediated induction of HIF-1α protein, as was activation of phosphoinositide 3-kinase and mitogen-activated protein kinase pathways. In conclusion, we demonstrated that CSE and CS induced HIF-1 activation in vitro and in vivo, respectively. The evidence warrants further investigation to indicate that HIF-1 plays an important role in CS-induced gene expression, which is deeply involved in pulmonary cellular stress and small airway remodelling. |
著作権等: | © The Author(s) 2016. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
URI: | http://hdl.handle.net/2433/217026 |
DOI(出版社版): | 10.1038/srep34424 |
PubMed ID: | 27680676 |
出現コレクション: | 学術雑誌掲載論文等 |
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