Structural, functional, and molecular impact on the cardiovascular system in ApoE-/- mice exposed to aerosol from candidate modified risk tobacco products, Carbon Heated Tobacco Product 1.2 and Tobacco Heating System 2.2, compared with cigarette smoke
To investigate the molecular, structural, and functional impact of aerosols from candidate modified risk tobacco products (cMRTP), the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of mainstream cigarette smoke (CS) on the cardiovascular system of...
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creator | Szostak, Justyna Titz, Bjoern Schlage, Walter K. Guedj, Emmanuel Sewer, Alain Phillips, Blaine Leroy, Patrice Buettner, Ansgar Neau, Laurent Trivedi, Keyur Martin, Florian Ivanov, Nikolai V. Vanscheeuwijck, Patrick Peitsch, Manuel C. Hoeng, Julia |
description | To investigate the molecular, structural, and functional impact of aerosols from candidate modified risk tobacco products (cMRTP), the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of mainstream cigarette smoke (CS) on the cardiovascular system of ApoE-/- mice.
Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from the 3R4F reference cigarette for up to 6 months at matching nicotine concentrations. A Cessation and a Switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated by echocardiographic, histopathological, immunohistochemical, and transcriptomics analyses.
Continuous exposure to cMRTP aerosols did not affect atherosclerosis progression, heart function, left ventricular (LV) structure, or the cardiovascular transcriptome. Exposure to 3R4F CS triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart LV hypertrophy, and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, the structural, functional, and molecular changes caused by 3R4F CS were improved in the smoking cessation and switching groups.
Exposure to cMRTP aerosols lacked most of the CS exposure-related functional, structural, and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused similar recovery from the 3R4F CS effects in the ApoE-/- model, with no further acceleration of plaque progression beyond the aging-related rate.
•cMRTP aerosols induce less atherosclerotic plaque formation than CS.•cMRTP aerosols induce lower molecular changes in the aorta and heart tissues than CS.•Smoking cessation reverses gene expression changes in the heart ventricle and aorta. |
doi_str_mv | 10.1016/j.cbi.2019.108887 |
format | Article |
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Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from the 3R4F reference cigarette for up to 6 months at matching nicotine concentrations. A Cessation and a Switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated by echocardiographic, histopathological, immunohistochemical, and transcriptomics analyses.
Continuous exposure to cMRTP aerosols did not affect atherosclerosis progression, heart function, left ventricular (LV) structure, or the cardiovascular transcriptome. Exposure to 3R4F CS triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart LV hypertrophy, and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, the structural, functional, and molecular changes caused by 3R4F CS were improved in the smoking cessation and switching groups.
Exposure to cMRTP aerosols lacked most of the CS exposure-related functional, structural, and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused similar recovery from the 3R4F CS effects in the ApoE-/- model, with no further acceleration of plaque progression beyond the aging-related rate.
•cMRTP aerosols induce less atherosclerotic plaque formation than CS.•cMRTP aerosols induce lower molecular changes in the aorta and heart tissues than CS.•Smoking cessation reverses gene expression changes in the heart ventricle and aorta.</description><identifier>ISSN: 0009-2797</identifier><identifier>ISSN: 1872-7786</identifier><identifier>EISSN: 1872-7786</identifier><identifier>DOI: 10.1016/j.cbi.2019.108887</identifier><identifier>PMID: 31705857</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Aerosols - adverse effects ; Ahr ; Animals ; Aorta, Thoracic - drug effects ; ApoE-/- mice ; Apolipoproteins E - metabolism ; Atherosclerosis ; Atherosclerosis - metabolism ; Candidate modified-risk tobacco products ; Carbon - adverse effects ; Cardiovascular System - drug effects ; Cardiovascular System - metabolism ; Cigarette smoke ; Female ; Heart ventricle dysfunction ; Heating - adverse effects ; Inhalation Exposure - adverse effects ; Lung - drug effects ; Lung - metabolism ; Mice ; Smoke - adverse effects ; Smoking - adverse effects ; Tobacco Products - adverse effects ; Transcriptome - drug effects ; Xenobiotic metabolism</subject><ispartof>Chemico-biological interactions, 2020-01, Vol.315, p.108887, Article 108887</ispartof><rights>2019</rights><rights>Copyright © 2019. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c353t-71808aa9bac3e7772db79ed37bf40c76aff81253d44255101e456cae404938f93</citedby><cites>FETCH-LOGICAL-c353t-71808aa9bac3e7772db79ed37bf40c76aff81253d44255101e456cae404938f93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0009279719310026$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31705857$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Szostak, Justyna</creatorcontrib><creatorcontrib>Titz, Bjoern</creatorcontrib><creatorcontrib>Schlage, Walter K.</creatorcontrib><creatorcontrib>Guedj, Emmanuel</creatorcontrib><creatorcontrib>Sewer, Alain</creatorcontrib><creatorcontrib>Phillips, Blaine</creatorcontrib><creatorcontrib>Leroy, Patrice</creatorcontrib><creatorcontrib>Buettner, Ansgar</creatorcontrib><creatorcontrib>Neau, Laurent</creatorcontrib><creatorcontrib>Trivedi, Keyur</creatorcontrib><creatorcontrib>Martin, Florian</creatorcontrib><creatorcontrib>Ivanov, Nikolai V.</creatorcontrib><creatorcontrib>Vanscheeuwijck, Patrick</creatorcontrib><creatorcontrib>Peitsch, Manuel C.</creatorcontrib><creatorcontrib>Hoeng, Julia</creatorcontrib><title>Structural, functional, and molecular impact on the cardiovascular system in ApoE-/- mice exposed to aerosol from candidate modified risk tobacco products, Carbon Heated Tobacco Product 1.2 and Tobacco Heating System 2.2, compared with cigarette smoke</title><title>Chemico-biological interactions</title><addtitle>Chem Biol Interact</addtitle><description>To investigate the molecular, structural, and functional impact of aerosols from candidate modified risk tobacco products (cMRTP), the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of mainstream cigarette smoke (CS) on the cardiovascular system of ApoE-/- mice.
Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from the 3R4F reference cigarette for up to 6 months at matching nicotine concentrations. A Cessation and a Switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated by echocardiographic, histopathological, immunohistochemical, and transcriptomics analyses.
Continuous exposure to cMRTP aerosols did not affect atherosclerosis progression, heart function, left ventricular (LV) structure, or the cardiovascular transcriptome. Exposure to 3R4F CS triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart LV hypertrophy, and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, the structural, functional, and molecular changes caused by 3R4F CS were improved in the smoking cessation and switching groups.
Exposure to cMRTP aerosols lacked most of the CS exposure-related functional, structural, and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused similar recovery from the 3R4F CS effects in the ApoE-/- model, with no further acceleration of plaque progression beyond the aging-related rate.
•cMRTP aerosols induce less atherosclerotic plaque formation than CS.•cMRTP aerosols induce lower molecular changes in the aorta and heart tissues than CS.•Smoking cessation reverses gene expression changes in the heart ventricle and aorta.</description><subject>Aerosols - adverse effects</subject><subject>Ahr</subject><subject>Animals</subject><subject>Aorta, Thoracic - drug effects</subject><subject>ApoE-/- mice</subject><subject>Apolipoproteins E - metabolism</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - metabolism</subject><subject>Candidate modified-risk tobacco products</subject><subject>Carbon - adverse effects</subject><subject>Cardiovascular System - drug effects</subject><subject>Cardiovascular System - metabolism</subject><subject>Cigarette smoke</subject><subject>Female</subject><subject>Heart ventricle dysfunction</subject><subject>Heating - adverse effects</subject><subject>Inhalation Exposure - adverse effects</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Mice</subject><subject>Smoke - adverse effects</subject><subject>Smoking - adverse effects</subject><subject>Tobacco Products - adverse effects</subject><subject>Transcriptome - drug effects</subject><subject>Xenobiotic metabolism</subject><issn>0009-2797</issn><issn>1872-7786</issn><issn>1872-7786</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1v1DAQjRCILoUfwAX5yGGT-iOJE3GqVoUiVQKp5Ww59qT1NomD7bT0t3Nhlmw5crLH896bN35Z9p7RglFWn-0L07mCU9Zi3TSNfJFtWCN5LmVTv8w2lNI257KVJ9mbGPdYUl7S19mJYJJWTSU32e_rFBaTlqCHLemXySTnp8NdT5aMfgCzDDoQN87aJOInku6AGB2s8w86rs34FBOMxE3kfPYX-VlORmeAwK_ZR7AkeaIh-OgH0gc_InuyzuoEqG9d7xASXLxHXKeN8WQO3qKluCU7HToceQkItuTm2P--9gkr-F-Xz-8HmJtuyfVqhxd8S4xH4wHJjy7dEeNusUg4OY7-Ht5mr3o9RHh3PE-zH58vbnaX-dW3L19351e5EZVIuWQNbbRucYoAKSW3nWzBCtn1JTWy1n3fMF4JW5a8qjAYKKvaaChp2Yqmb8Vp9nHVxc1-LhCTGl00MAx6Ar9ExQUTopK0LhHKVqjBD4sBejUHN-rwpBhVh8zVXmHm6pC5WjNHzoej_NKNYP8xnkNGwKcVALjkg4OgonEwGbAugEnKevcf-T-Q8MAi</recordid><startdate>20200105</startdate><enddate>20200105</enddate><creator>Szostak, Justyna</creator><creator>Titz, Bjoern</creator><creator>Schlage, Walter K.</creator><creator>Guedj, Emmanuel</creator><creator>Sewer, Alain</creator><creator>Phillips, Blaine</creator><creator>Leroy, Patrice</creator><creator>Buettner, Ansgar</creator><creator>Neau, Laurent</creator><creator>Trivedi, Keyur</creator><creator>Martin, Florian</creator><creator>Ivanov, Nikolai V.</creator><creator>Vanscheeuwijck, Patrick</creator><creator>Peitsch, Manuel C.</creator><creator>Hoeng, Julia</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20200105</creationdate><title>Structural, functional, and molecular impact on the cardiovascular system in ApoE-/- mice exposed to aerosol from candidate modified risk tobacco products, Carbon Heated Tobacco Product 1.2 and Tobacco Heating System 2.2, compared with cigarette smoke</title><author>Szostak, Justyna ; Titz, Bjoern ; Schlage, Walter K. ; Guedj, Emmanuel ; Sewer, Alain ; Phillips, Blaine ; Leroy, Patrice ; Buettner, Ansgar ; Neau, Laurent ; Trivedi, Keyur ; Martin, Florian ; Ivanov, Nikolai V. ; Vanscheeuwijck, Patrick ; Peitsch, Manuel C. ; Hoeng, Julia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c353t-71808aa9bac3e7772db79ed37bf40c76aff81253d44255101e456cae404938f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aerosols - adverse effects</topic><topic>Ahr</topic><topic>Animals</topic><topic>Aorta, Thoracic - drug effects</topic><topic>ApoE-/- mice</topic><topic>Apolipoproteins E - metabolism</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - metabolism</topic><topic>Candidate modified-risk tobacco products</topic><topic>Carbon - adverse effects</topic><topic>Cardiovascular System - drug effects</topic><topic>Cardiovascular System - metabolism</topic><topic>Cigarette smoke</topic><topic>Female</topic><topic>Heart ventricle dysfunction</topic><topic>Heating - adverse effects</topic><topic>Inhalation Exposure - adverse effects</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>Mice</topic><topic>Smoke - adverse effects</topic><topic>Smoking - adverse effects</topic><topic>Tobacco Products - adverse effects</topic><topic>Transcriptome - drug effects</topic><topic>Xenobiotic metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Szostak, Justyna</creatorcontrib><creatorcontrib>Titz, Bjoern</creatorcontrib><creatorcontrib>Schlage, Walter K.</creatorcontrib><creatorcontrib>Guedj, Emmanuel</creatorcontrib><creatorcontrib>Sewer, Alain</creatorcontrib><creatorcontrib>Phillips, Blaine</creatorcontrib><creatorcontrib>Leroy, Patrice</creatorcontrib><creatorcontrib>Buettner, Ansgar</creatorcontrib><creatorcontrib>Neau, Laurent</creatorcontrib><creatorcontrib>Trivedi, Keyur</creatorcontrib><creatorcontrib>Martin, Florian</creatorcontrib><creatorcontrib>Ivanov, Nikolai V.</creatorcontrib><creatorcontrib>Vanscheeuwijck, Patrick</creatorcontrib><creatorcontrib>Peitsch, Manuel C.</creatorcontrib><creatorcontrib>Hoeng, Julia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Chemico-biological interactions</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Szostak, Justyna</au><au>Titz, Bjoern</au><au>Schlage, Walter K.</au><au>Guedj, Emmanuel</au><au>Sewer, Alain</au><au>Phillips, Blaine</au><au>Leroy, Patrice</au><au>Buettner, Ansgar</au><au>Neau, Laurent</au><au>Trivedi, Keyur</au><au>Martin, Florian</au><au>Ivanov, Nikolai V.</au><au>Vanscheeuwijck, Patrick</au><au>Peitsch, Manuel C.</au><au>Hoeng, Julia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Structural, functional, and molecular impact on the cardiovascular system in ApoE-/- mice exposed to aerosol from candidate modified risk tobacco products, Carbon Heated Tobacco Product 1.2 and Tobacco Heating System 2.2, compared with cigarette smoke</atitle><jtitle>Chemico-biological interactions</jtitle><addtitle>Chem Biol Interact</addtitle><date>2020-01-05</date><risdate>2020</risdate><volume>315</volume><spage>108887</spage><pages>108887-</pages><artnum>108887</artnum><issn>0009-2797</issn><issn>1872-7786</issn><eissn>1872-7786</eissn><abstract>To investigate the molecular, structural, and functional impact of aerosols from candidate modified risk tobacco products (cMRTP), the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of mainstream cigarette smoke (CS) on the cardiovascular system of ApoE-/- mice.
Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from the 3R4F reference cigarette for up to 6 months at matching nicotine concentrations. A Cessation and a Switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated by echocardiographic, histopathological, immunohistochemical, and transcriptomics analyses.
Continuous exposure to cMRTP aerosols did not affect atherosclerosis progression, heart function, left ventricular (LV) structure, or the cardiovascular transcriptome. Exposure to 3R4F CS triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart LV hypertrophy, and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, the structural, functional, and molecular changes caused by 3R4F CS were improved in the smoking cessation and switching groups.
Exposure to cMRTP aerosols lacked most of the CS exposure-related functional, structural, and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused similar recovery from the 3R4F CS effects in the ApoE-/- model, with no further acceleration of plaque progression beyond the aging-related rate.
•cMRTP aerosols induce less atherosclerotic plaque formation than CS.•cMRTP aerosols induce lower molecular changes in the aorta and heart tissues than CS.•Smoking cessation reverses gene expression changes in the heart ventricle and aorta.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>31705857</pmid><doi>10.1016/j.cbi.2019.108887</doi></addata></record> |
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subjects | Aerosols - adverse effects Ahr Animals Aorta, Thoracic - drug effects ApoE-/- mice Apolipoproteins E - metabolism Atherosclerosis Atherosclerosis - metabolism Candidate modified-risk tobacco products Carbon - adverse effects Cardiovascular System - drug effects Cardiovascular System - metabolism Cigarette smoke Female Heart ventricle dysfunction Heating - adverse effects Inhalation Exposure - adverse effects Lung - drug effects Lung - metabolism Mice Smoke - adverse effects Smoking - adverse effects Tobacco Products - adverse effects Transcriptome - drug effects Xenobiotic metabolism |
title | Structural, functional, and molecular impact on the cardiovascular system in ApoE-/- mice exposed to aerosol from candidate modified risk tobacco products, Carbon Heated Tobacco Product 1.2 and Tobacco Heating System 2.2, compared with cigarette smoke |
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