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Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase

Pulmonary fibrosis (PF) is one of the most prevalent causes of death following paraquat (PQ) poisoning. As demonstrated in previous studies by the present authors, epithelial-to-mesenchymal transition (EMT) is associated with PQ-induced PF. In addition, hypoxia-inducible factor-1α (HIF-1α) and lysyl...

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Autores principales: Lu, Jian, Qian, Yongbing, Jin, Wei, Tian, Rui, Zhu, Yong, Wang, Jinfeng, Meng, Xiaoxiao, Wang, Ruilan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5792814/
https://www.ncbi.nlm.nih.gov/pubmed/29467842
http://dx.doi.org/10.3892/etm.2017.5677
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author Lu, Jian
Qian, Yongbing
Jin, Wei
Tian, Rui
Zhu, Yong
Wang, Jinfeng
Meng, Xiaoxiao
Wang, Ruilan
author_facet Lu, Jian
Qian, Yongbing
Jin, Wei
Tian, Rui
Zhu, Yong
Wang, Jinfeng
Meng, Xiaoxiao
Wang, Ruilan
author_sort Lu, Jian
collection PubMed
description Pulmonary fibrosis (PF) is one of the most prevalent causes of death following paraquat (PQ) poisoning. As demonstrated in previous studies by the present authors, epithelial-to-mesenchymal transition (EMT) is associated with PQ-induced PF. In addition, hypoxia-inducible factor-1α (HIF-1α) and lysyl oxidase (LOX) promote EMT following PQ poisoning. However, the association between HIF-1α- and LOX-mediated regulation of EMT remains unclear. The present study investigated the association between HIF-1α and LOX with regard to PQ-induced EMT. A549 and RLE-6TN cells were treated with PQ, and HIF-1α and LOX expression was silenced with short interfering RNAs. Changes in the expression of HIF-1α, LOX, β-catenin and EMT-related makers were detected using real-time quantitative polymerase chain reaction, immunofluorescence, and western blotting. HIF-1α and LOX were associated with PQ-induced EMT, and their expression levels were significantly increased (P<0.05). LOX expression was significantly decreased following PQ poisoning when HIF-1α expression was inhibited (P<0.05). However, the level of HIF-1α did not change significantly when LOX was silenced. The expression level of β-catenin and the degree of EMT were significantly decreased following HIF-1α and LOX silencing in both cell lines (P<0.05). The association between HIF-1α and LOX in regulating EMT during PQ-induced PF may be unidirectional. HIF-1α may regulate PQ-induced EMT through the LOX/β-catenin pathway.
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spelling pubmed-57928142018-02-21 Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase Lu, Jian Qian, Yongbing Jin, Wei Tian, Rui Zhu, Yong Wang, Jinfeng Meng, Xiaoxiao Wang, Ruilan Exp Ther Med Articles Pulmonary fibrosis (PF) is one of the most prevalent causes of death following paraquat (PQ) poisoning. As demonstrated in previous studies by the present authors, epithelial-to-mesenchymal transition (EMT) is associated with PQ-induced PF. In addition, hypoxia-inducible factor-1α (HIF-1α) and lysyl oxidase (LOX) promote EMT following PQ poisoning. However, the association between HIF-1α- and LOX-mediated regulation of EMT remains unclear. The present study investigated the association between HIF-1α and LOX with regard to PQ-induced EMT. A549 and RLE-6TN cells were treated with PQ, and HIF-1α and LOX expression was silenced with short interfering RNAs. Changes in the expression of HIF-1α, LOX, β-catenin and EMT-related makers were detected using real-time quantitative polymerase chain reaction, immunofluorescence, and western blotting. HIF-1α and LOX were associated with PQ-induced EMT, and their expression levels were significantly increased (P<0.05). LOX expression was significantly decreased following PQ poisoning when HIF-1α expression was inhibited (P<0.05). However, the level of HIF-1α did not change significantly when LOX was silenced. The expression level of β-catenin and the degree of EMT were significantly decreased following HIF-1α and LOX silencing in both cell lines (P<0.05). The association between HIF-1α and LOX in regulating EMT during PQ-induced PF may be unidirectional. HIF-1α may regulate PQ-induced EMT through the LOX/β-catenin pathway. D.A. Spandidos 2018-03 2017-12-22 /pmc/articles/PMC5792814/ /pubmed/29467842 http://dx.doi.org/10.3892/etm.2017.5677 Text en Copyright: © Lu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Lu, Jian
Qian, Yongbing
Jin, Wei
Tian, Rui
Zhu, Yong
Wang, Jinfeng
Meng, Xiaoxiao
Wang, Ruilan
Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase
title Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase
title_full Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase
title_fullStr Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase
title_full_unstemmed Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase
title_short Hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase
title_sort hypoxia-inducible factor-1α regulates epithelial-to-mesenchymal transition in paraquat-induced pulmonary fibrosis by activating lysyl oxidase
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5792814/
https://www.ncbi.nlm.nih.gov/pubmed/29467842
http://dx.doi.org/10.3892/etm.2017.5677
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