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Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling
Endoscopic implantation of medical devices for the treatment of lung diseases, including airway stents, unidirectional valves and coils, is readily used to treat central airway disease and emphysema. However, granulation and fibrotic tissue formation impairs treatment effectiveness. To date little i...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10366254/ https://www.ncbi.nlm.nih.gov/pubmed/37486435 http://dx.doi.org/10.1007/s10856-023-06742-2 |
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author | Pouwels, Simon D. Sigaeva, Alina de Boer, Shanna Eichhorn, Ilse A. Koll, Lisanne Kuipers, Jeroen Schirhagl, Romana Heijink, Irene H. Burgess, Janette K. Slebos, Dirk-Jan |
author_facet | Pouwels, Simon D. Sigaeva, Alina de Boer, Shanna Eichhorn, Ilse A. Koll, Lisanne Kuipers, Jeroen Schirhagl, Romana Heijink, Irene H. Burgess, Janette K. Slebos, Dirk-Jan |
author_sort | Pouwels, Simon D. |
collection | PubMed |
description | Endoscopic implantation of medical devices for the treatment of lung diseases, including airway stents, unidirectional valves and coils, is readily used to treat central airway disease and emphysema. However, granulation and fibrotic tissue formation impairs treatment effectiveness. To date little is known about the interaction between implanted devices, often made from metals, such as nickel, titanium or nitinol, and cells in the airways. Here, we study the response of lung epithelial cells and fibroblasts to implant device materials. The adhesion and proliferation of bronchial epithelial cells and lung fibroblasts upon exposure to 10 × 3 × 1 mm pieces of nickel, titanium or nitinol is examined using light and scanning electron microscopy. Pro-inflammatory cytokine mRNA expression and release, signaling kinase activity and intracellular free radical production are assessed. Nitinol, and to a lesser extent nickel and titanium, surfaces support the attachment and growth of lung epithelial cells. Nitinol induces a rapid and significant alteration of kinase activity. Cells directly exposed to nickel or titanium produce free radicals, but those exposed to nitinol do not. The response of lung epithelial cells and fibroblasts depends on the metal type to which they are exposed. Nitinol induces cellular surface growth and the induction of kinase activity, while exposure of lung epithelial cells to nickel and titanium induces free radical production, but nitinol does not. GRAPHICAL ABSTRACT: [Image: see text] |
format | Online Article Text |
id | pubmed-10366254 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-103662542023-07-26 Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling Pouwels, Simon D. Sigaeva, Alina de Boer, Shanna Eichhorn, Ilse A. Koll, Lisanne Kuipers, Jeroen Schirhagl, Romana Heijink, Irene H. Burgess, Janette K. Slebos, Dirk-Jan J Mater Sci Mater Med S.I.: Biomaterial-Tissue Interaction in Humans Endoscopic implantation of medical devices for the treatment of lung diseases, including airway stents, unidirectional valves and coils, is readily used to treat central airway disease and emphysema. However, granulation and fibrotic tissue formation impairs treatment effectiveness. To date little is known about the interaction between implanted devices, often made from metals, such as nickel, titanium or nitinol, and cells in the airways. Here, we study the response of lung epithelial cells and fibroblasts to implant device materials. The adhesion and proliferation of bronchial epithelial cells and lung fibroblasts upon exposure to 10 × 3 × 1 mm pieces of nickel, titanium or nitinol is examined using light and scanning electron microscopy. Pro-inflammatory cytokine mRNA expression and release, signaling kinase activity and intracellular free radical production are assessed. Nitinol, and to a lesser extent nickel and titanium, surfaces support the attachment and growth of lung epithelial cells. Nitinol induces a rapid and significant alteration of kinase activity. Cells directly exposed to nickel or titanium produce free radicals, but those exposed to nitinol do not. The response of lung epithelial cells and fibroblasts depends on the metal type to which they are exposed. Nitinol induces cellular surface growth and the induction of kinase activity, while exposure of lung epithelial cells to nickel and titanium induces free radical production, but nitinol does not. GRAPHICAL ABSTRACT: [Image: see text] Springer US 2023-07-24 2023 /pmc/articles/PMC10366254/ /pubmed/37486435 http://dx.doi.org/10.1007/s10856-023-06742-2 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | S.I.: Biomaterial-Tissue Interaction in Humans Pouwels, Simon D. Sigaeva, Alina de Boer, Shanna Eichhorn, Ilse A. Koll, Lisanne Kuipers, Jeroen Schirhagl, Romana Heijink, Irene H. Burgess, Janette K. Slebos, Dirk-Jan Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling |
title | Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling |
title_full | Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling |
title_fullStr | Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling |
title_full_unstemmed | Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling |
title_short | Host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling |
title_sort | host–device interactions: exposure of lung epithelial cells and fibroblasts to nickel, titanium, or nitinol affect proliferation, reactive oxygen species production, and cellular signaling |
topic | S.I.: Biomaterial-Tissue Interaction in Humans |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10366254/ https://www.ncbi.nlm.nih.gov/pubmed/37486435 http://dx.doi.org/10.1007/s10856-023-06742-2 |
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