E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted Angiogenesis
Cardiovascular disease (CVD) is a leading cause of mortality worldwide, with cigarette smoking being a major preventable risk factor. Smoking cessation can be difficult due to the addictive nature of nicotine and the withdrawal symptoms following cessation. Electronic cigarettes (e-Cigs) have emerge...
| Main Authors: | , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2023-03-01
|
| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/24/7/6378 |
| _version_ | 1797607809838219264 |
|---|---|
| author | Michael Chhor Esra Tulpar Tara Nguyen Charles G. Cranfield Catherine A. Gorrie Yik Lung Chan Hui Chen Brian G. Oliver Lana McClements Kristine C. McGrath |
| author_facet | Michael Chhor Esra Tulpar Tara Nguyen Charles G. Cranfield Catherine A. Gorrie Yik Lung Chan Hui Chen Brian G. Oliver Lana McClements Kristine C. McGrath |
| author_sort | Michael Chhor |
| collection | DOAJ |
| description | Cardiovascular disease (CVD) is a leading cause of mortality worldwide, with cigarette smoking being a major preventable risk factor. Smoking cessation can be difficult due to the addictive nature of nicotine and the withdrawal symptoms following cessation. Electronic cigarettes (e-Cigs) have emerged as an alternative smoking cessation device, which has been increasingly used by non-smokers; however, the cardiovascular effects surrounding the use of e-Cigs remains unclear. This study aimed to investigate the effects of e-Cig aerosol condensate (EAC) (0 mg and 18 mg nicotine) in vitro on human coronary artery endothelial cells (HCAEC) and in vivo on the cardiovascular system using a mouse model of ‘e-vaping’. In vitro results show a decrease in cell viability of HCAEC when exposed to EAC either directly or after exposure to conditioned lung cell media (<i>p</i> < 0.05 vs. control). Reactive oxygen species were increased in HCAEC when exposed to EAC directly or after exposure to conditioned lung cell media (<i>p</i> < 0.0001 vs. control). ICAM-1 protein expression levels were increased after exposure to conditioned lung cell media (18 mg vs. control, <i>p</i> < 0.01). Ex vivo results show an increase in the mRNA levels of anti-angiogenic marker, <i>FKBPL</i> (<i>p</i> < 0.05 vs. sham), and endothelial cell adhesion molecule involved in barrier function, <i>ICAM-1</i> (<i>p</i> < 0.05 vs. sham) in murine hearts following exposure to electronic cigarette aerosol treatment containing a higher amount of nicotine. Immunohistochemistry also revealed an upregulation of FKBPL and ICAM-1 protein expression levels. This study showed that despite e-Cigs being widely used for tobacco smoking cessation, these can negatively impact endothelial cell health with a potential to lead to the development of cardiovascular disease. |
| first_indexed | 2024-03-11T05:34:55Z |
| format | Article |
| id | doaj.art-72d89cac906f4ea5aa0d318a27b3d894 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-11T05:34:55Z |
| publishDate | 2023-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-72d89cac906f4ea5aa0d318a27b3d8942023-11-17T16:50:20ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-03-01247637810.3390/ijms24076378E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted AngiogenesisMichael Chhor0Esra Tulpar1Tara Nguyen2Charles G. Cranfield3Catherine A. Gorrie4Yik Lung Chan5Hui Chen6Brian G. Oliver7Lana McClements8Kristine C. McGrath9School of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW 2007, AustraliaCardiovascular disease (CVD) is a leading cause of mortality worldwide, with cigarette smoking being a major preventable risk factor. Smoking cessation can be difficult due to the addictive nature of nicotine and the withdrawal symptoms following cessation. Electronic cigarettes (e-Cigs) have emerged as an alternative smoking cessation device, which has been increasingly used by non-smokers; however, the cardiovascular effects surrounding the use of e-Cigs remains unclear. This study aimed to investigate the effects of e-Cig aerosol condensate (EAC) (0 mg and 18 mg nicotine) in vitro on human coronary artery endothelial cells (HCAEC) and in vivo on the cardiovascular system using a mouse model of ‘e-vaping’. In vitro results show a decrease in cell viability of HCAEC when exposed to EAC either directly or after exposure to conditioned lung cell media (<i>p</i> < 0.05 vs. control). Reactive oxygen species were increased in HCAEC when exposed to EAC directly or after exposure to conditioned lung cell media (<i>p</i> < 0.0001 vs. control). ICAM-1 protein expression levels were increased after exposure to conditioned lung cell media (18 mg vs. control, <i>p</i> < 0.01). Ex vivo results show an increase in the mRNA levels of anti-angiogenic marker, <i>FKBPL</i> (<i>p</i> < 0.05 vs. sham), and endothelial cell adhesion molecule involved in barrier function, <i>ICAM-1</i> (<i>p</i> < 0.05 vs. sham) in murine hearts following exposure to electronic cigarette aerosol treatment containing a higher amount of nicotine. Immunohistochemistry also revealed an upregulation of FKBPL and ICAM-1 protein expression levels. This study showed that despite e-Cigs being widely used for tobacco smoking cessation, these can negatively impact endothelial cell health with a potential to lead to the development of cardiovascular disease.https://www.mdpi.com/1422-0067/24/7/6378e-vapingcardiovascular diseasesmokingnicotineatherosclerosis |
| spellingShingle | Michael Chhor Esra Tulpar Tara Nguyen Charles G. Cranfield Catherine A. Gorrie Yik Lung Chan Hui Chen Brian G. Oliver Lana McClements Kristine C. McGrath E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted Angiogenesis International Journal of Molecular Sciences e-vaping cardiovascular disease smoking nicotine atherosclerosis |
| title | E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted Angiogenesis |
| title_full | E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted Angiogenesis |
| title_fullStr | E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted Angiogenesis |
| title_full_unstemmed | E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted Angiogenesis |
| title_short | E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted Angiogenesis |
| title_sort | e cigarette aerosol condensate leads to impaired coronary endothelial cell health and restricted angiogenesis |
| topic | e-vaping cardiovascular disease smoking nicotine atherosclerosis |
| url | https://www.mdpi.com/1422-0067/24/7/6378 |
| work_keys_str_mv | AT michaelchhor ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT esratulpar ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT taranguyen ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT charlesgcranfield ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT catherineagorrie ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT yiklungchan ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT huichen ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT briangoliver ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT lanamcclements ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis AT kristinecmcgrath ecigaretteaerosolcondensateleadstoimpairedcoronaryendothelialcellhealthandrestrictedangiogenesis |