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Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture
BACKGROUND: It is generally acknowledged that e-cigarettes are unlikely to be as harmful as conventional cigarettes, but there is little data that quantifies their relative harms. We investigated the biological response to e-cigarette aerosol exposure (versus conventional cigarette smoke exposure) a...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4907307/ https://www.ncbi.nlm.nih.gov/pubmed/27137404 http://dx.doi.org/10.1016/j.drugalcdep.2016.04.020 |
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author | Teasdale, Jack E. Newby, Andrew C. Timpson, Nicholas J. Munafò, Marcus R. White, Stephen J. |
author_facet | Teasdale, Jack E. Newby, Andrew C. Timpson, Nicholas J. Munafò, Marcus R. White, Stephen J. |
author_sort | Teasdale, Jack E. |
collection | PubMed |
description | BACKGROUND: It is generally acknowledged that e-cigarettes are unlikely to be as harmful as conventional cigarettes, but there is little data that quantifies their relative harms. We investigated the biological response to e-cigarette aerosol exposure (versus conventional cigarette smoke exposure) at the cellular level, by exposing human coronary artery endothelial cells (HCAEC) to aqueous filtered extracts of e-cigarette aerosol or cigarette smoke and looking at gene expression changes consistent with a stress response. This included genes controlled by the oxidant-stress sensing transcription factor NFR2 (NFE2L2), and cytochrome P450 family members. METHODS: Cigarette smoke extract (CSE) was created using mainstream smoke from a single cigarette drawn through 10 ml of endothelial cell growth media MV2. Electronic cigarette aerosol extract (eCAE) was created using the same apparatus, using a constant power output of 10.8 w (4.2 V) and 18 mg/ml nicotine solution. eCAE was generated using 5 cycles of 5 s heat with at least 10 s in between each puff to allow the coil to cool, air being drawn through the device at 70 ml/minute. RESULTS: HCAEC responded to the noxious components in CSE, resulting in activation of NRF2 and upregulation of cytochrome p450. However, eCAE did not induce NRF2 nuclear localisation, upregulation of NRF2-activated genes, or the upregulation of cytochrome p450. CONCLUSIONS: The use of e-cigarettes as a substitute for conventional cigarettes is likely to reduce immediate tobacco-related harm, at least with respect to cardiovascular harms. |
format | Online Article Text |
id | pubmed-4907307 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-49073072016-06-22 Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture Teasdale, Jack E. Newby, Andrew C. Timpson, Nicholas J. Munafò, Marcus R. White, Stephen J. Drug Alcohol Depend Short Communication BACKGROUND: It is generally acknowledged that e-cigarettes are unlikely to be as harmful as conventional cigarettes, but there is little data that quantifies their relative harms. We investigated the biological response to e-cigarette aerosol exposure (versus conventional cigarette smoke exposure) at the cellular level, by exposing human coronary artery endothelial cells (HCAEC) to aqueous filtered extracts of e-cigarette aerosol or cigarette smoke and looking at gene expression changes consistent with a stress response. This included genes controlled by the oxidant-stress sensing transcription factor NFR2 (NFE2L2), and cytochrome P450 family members. METHODS: Cigarette smoke extract (CSE) was created using mainstream smoke from a single cigarette drawn through 10 ml of endothelial cell growth media MV2. Electronic cigarette aerosol extract (eCAE) was created using the same apparatus, using a constant power output of 10.8 w (4.2 V) and 18 mg/ml nicotine solution. eCAE was generated using 5 cycles of 5 s heat with at least 10 s in between each puff to allow the coil to cool, air being drawn through the device at 70 ml/minute. RESULTS: HCAEC responded to the noxious components in CSE, resulting in activation of NRF2 and upregulation of cytochrome p450. However, eCAE did not induce NRF2 nuclear localisation, upregulation of NRF2-activated genes, or the upregulation of cytochrome p450. CONCLUSIONS: The use of e-cigarettes as a substitute for conventional cigarettes is likely to reduce immediate tobacco-related harm, at least with respect to cardiovascular harms. Elsevier 2016-06-01 /pmc/articles/PMC4907307/ /pubmed/27137404 http://dx.doi.org/10.1016/j.drugalcdep.2016.04.020 Text en © 2016 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Short Communication Teasdale, Jack E. Newby, Andrew C. Timpson, Nicholas J. Munafò, Marcus R. White, Stephen J. Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture |
title | Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture |
title_full | Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture |
title_fullStr | Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture |
title_full_unstemmed | Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture |
title_short | Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture |
title_sort | cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture |
topic | Short Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4907307/ https://www.ncbi.nlm.nih.gov/pubmed/27137404 http://dx.doi.org/10.1016/j.drugalcdep.2016.04.020 |
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