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Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis
Lung fibrosis is a major complication in radiation-induced lung damage following thoracic radiotherapy, while the underlying mechanism has remained to be elucidated. The present study performed immunofluorescence and immunoblot assays on irradiated human pulmonary artery endothelial cells (HPAECs) w...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4838118/ https://www.ncbi.nlm.nih.gov/pubmed/27053172 http://dx.doi.org/10.3892/mmr.2016.5090 |
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author | CHOI, SEO-HYUN KIM, MISEON LEE, HAE-JUNE KIM, EUN-HO KIM, CHUN-HO LEE, YOON-JIN |
author_facet | CHOI, SEO-HYUN KIM, MISEON LEE, HAE-JUNE KIM, EUN-HO KIM, CHUN-HO LEE, YOON-JIN |
author_sort | CHOI, SEO-HYUN |
collection | PubMed |
description | Lung fibrosis is a major complication in radiation-induced lung damage following thoracic radiotherapy, while the underlying mechanism has remained to be elucidated. The present study performed immunofluorescence and immunoblot assays on irradiated human pulmonary artery endothelial cells (HPAECs) with or without pre-treatment with VAS2870, a novel NADPH oxidase (NOX) inhibitor, or small hairpin (sh)RNA against NOX1, -2 or -4. VAS2870 reduced the cellular reactive oxygen species content induced by 5 Gy radiation in HPAECs and inhibited phenotypic changes in fibrotic cells, including increased alpha smooth muscle actin and vimentin, and decreased CD31 and vascular endothelial cadherin expression. These fibrotic changes were significantly inhibited by treatment with NOX1 shRNA, but not by NOX2 or NOX4 shRNA. Next, the role of NOX1 in pulmonary fibrosis development was assessed in the lung tissues of C57BL/6J mice following thoracic irradiation using trichrome staining. Administration of an NOX1-specific inhibitor suppressed radiation-induced collagen deposition and fibroblastic changes in the endothelial cells (ECs) of these mice. The results suggested that radiation-induced pulmonary fibrosis may be efficiently reduced by specific inhibition of NOX1, an effect mediated by reduction of fibrotic changes of ECs. |
format | Online Article Text |
id | pubmed-4838118 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-48381182016-04-21 Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis CHOI, SEO-HYUN KIM, MISEON LEE, HAE-JUNE KIM, EUN-HO KIM, CHUN-HO LEE, YOON-JIN Mol Med Rep Articles Lung fibrosis is a major complication in radiation-induced lung damage following thoracic radiotherapy, while the underlying mechanism has remained to be elucidated. The present study performed immunofluorescence and immunoblot assays on irradiated human pulmonary artery endothelial cells (HPAECs) with or without pre-treatment with VAS2870, a novel NADPH oxidase (NOX) inhibitor, or small hairpin (sh)RNA against NOX1, -2 or -4. VAS2870 reduced the cellular reactive oxygen species content induced by 5 Gy radiation in HPAECs and inhibited phenotypic changes in fibrotic cells, including increased alpha smooth muscle actin and vimentin, and decreased CD31 and vascular endothelial cadherin expression. These fibrotic changes were significantly inhibited by treatment with NOX1 shRNA, but not by NOX2 or NOX4 shRNA. Next, the role of NOX1 in pulmonary fibrosis development was assessed in the lung tissues of C57BL/6J mice following thoracic irradiation using trichrome staining. Administration of an NOX1-specific inhibitor suppressed radiation-induced collagen deposition and fibroblastic changes in the endothelial cells (ECs) of these mice. The results suggested that radiation-induced pulmonary fibrosis may be efficiently reduced by specific inhibition of NOX1, an effect mediated by reduction of fibrotic changes of ECs. D.A. Spandidos 2016-05 2016-04-05 /pmc/articles/PMC4838118/ /pubmed/27053172 http://dx.doi.org/10.3892/mmr.2016.5090 Text en Copyright: © Choi 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 CHOI, SEO-HYUN KIM, MISEON LEE, HAE-JUNE KIM, EUN-HO KIM, CHUN-HO LEE, YOON-JIN Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis |
title | Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis |
title_full | Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis |
title_fullStr | Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis |
title_full_unstemmed | Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis |
title_short | Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis |
title_sort | effects of nox1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4838118/ https://www.ncbi.nlm.nih.gov/pubmed/27053172 http://dx.doi.org/10.3892/mmr.2016.5090 |
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