Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE −/− mice exposed to diesel exhaust particles

Abstract Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the...

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Main Authors: Inkyo Jung, Yoon Jin Cho, Minhan Park, Kihong Park, Seung Hee Lee, Won-Ho Kim, Hyuk Jeong, Ji Eun Lee, Geun-Young Kim
Format: Article
Language:English
Published: Nature Portfolio 2023-12-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-023-49790-y
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author Inkyo Jung
Yoon Jin Cho
Minhan Park
Kihong Park
Seung Hee Lee
Won-Ho Kim
Hyuk Jeong
Ji Eun Lee
Geun-Young Kim
author_facet Inkyo Jung
Yoon Jin Cho
Minhan Park
Kihong Park
Seung Hee Lee
Won-Ho Kim
Hyuk Jeong
Ji Eun Lee
Geun-Young Kim
author_sort Inkyo Jung
collection DOAJ
description Abstract Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the in vivo effects of diesel exhaust particles (DEP) on the heart and the molecular mechanisms of DEP-induced heart dysfunction have not been investigated. In the current study, we attempted to identify the proteomic signatures of heart fibrosis caused by diesel exhaust particles (DEP) in CVDs-prone apolipoprotein E knockout (ApoE −/− ) mice model using tandem mass tag (TMT)-based quantitative proteomic analysis. DEP exposure induced mild heart fibrosis in ApoE −/− mice compared with severe heart fibrosis in ApoE −/− mice that were treated with CVDs-inducing peptide, angiotensin II. TMT-based quantitative proteomic analysis of heart tissues between PBS- and DEP-treated ApoE −/− mice revealed significant upregulation of proteins associated with platelet activation and TGFβ-dependent pathways. Our data suggest that DEP exposure could induce heart fibrosis, potentially via platelet-related pathways and TGFβ induction, causing cardiac fibrosis and dysfunction.
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spelling doaj.art-2fd064de5bcb4743af14354dcfd1f7f52023-12-24T12:19:11ZengNature PortfolioScientific Reports2045-23222023-12-0113111510.1038/s41598-023-49790-yProteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE −/− mice exposed to diesel exhaust particlesInkyo Jung0Yoon Jin Cho1Minhan Park2Kihong Park3Seung Hee Lee4Won-Ho Kim5Hyuk Jeong6Ji Eun Lee7Geun-Young Kim8Division of Cardiovascular Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of HealthChemical and Biological Integrative Research Center, Biomedical Research Division, Korea Institute of Science and TechnologySchool of Earth Science and Environmental Engineering, Gwangju Institute of Science and TechnologySchool of Earth Science and Environmental Engineering, Gwangju Institute of Science and TechnologyDivision of Cardiovascular Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of HealthDivision of Cardiovascular Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of HealthDepartment of Chemistry, Sookmyung Women’s UniversityChemical and Biological Integrative Research Center, Biomedical Research Division, Korea Institute of Science and TechnologyDivision of Cardiovascular Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of HealthAbstract Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the in vivo effects of diesel exhaust particles (DEP) on the heart and the molecular mechanisms of DEP-induced heart dysfunction have not been investigated. In the current study, we attempted to identify the proteomic signatures of heart fibrosis caused by diesel exhaust particles (DEP) in CVDs-prone apolipoprotein E knockout (ApoE −/− ) mice model using tandem mass tag (TMT)-based quantitative proteomic analysis. DEP exposure induced mild heart fibrosis in ApoE −/− mice compared with severe heart fibrosis in ApoE −/− mice that were treated with CVDs-inducing peptide, angiotensin II. TMT-based quantitative proteomic analysis of heart tissues between PBS- and DEP-treated ApoE −/− mice revealed significant upregulation of proteins associated with platelet activation and TGFβ-dependent pathways. Our data suggest that DEP exposure could induce heart fibrosis, potentially via platelet-related pathways and TGFβ induction, causing cardiac fibrosis and dysfunction.https://doi.org/10.1038/s41598-023-49790-y
spellingShingle Inkyo Jung
Yoon Jin Cho
Minhan Park
Kihong Park
Seung Hee Lee
Won-Ho Kim
Hyuk Jeong
Ji Eun Lee
Geun-Young Kim
Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE −/− mice exposed to diesel exhaust particles
Scientific Reports
title Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE −/− mice exposed to diesel exhaust particles
title_full Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE −/− mice exposed to diesel exhaust particles
title_fullStr Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE −/− mice exposed to diesel exhaust particles
title_full_unstemmed Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE −/− mice exposed to diesel exhaust particles
title_short Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE −/− mice exposed to diesel exhaust particles
title_sort proteomic analysis reveals activation of platelet and fibrosis related pathways in hearts of apoe mice exposed to diesel exhaust particles
url https://doi.org/10.1038/s41598-023-49790-y
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