Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution
Inhalation of air pollution small particle matter (PM) is a leading cause of cardiovascular (CV) disease. Exposure to PMs causes endothelial cell (EC) dysfunction as evidenced by nitric oxide (NO) synthase uncoupling, vasoconstriction and inflammation. Eicosapentaenoic acid (EPA) has been shown to m...
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| Veröffentlicht in: | Biomedicine & pharmacotherapy 2023-06, Vol.162, p.114629, Article 114629 |
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| creator | Sherratt, Samuel C.R. Libby, Peter Dawoud, Hazem Bhatt, Deepak L. Malinski, Tadeusz Mason, R. Preston |
| description | Inhalation of air pollution small particle matter (PM) is a leading cause of cardiovascular (CV) disease. Exposure to PMs causes endothelial cell (EC) dysfunction as evidenced by nitric oxide (NO) synthase uncoupling, vasoconstriction and inflammation. Eicosapentaenoic acid (EPA) has been shown to mitigate PM-induced adverse cardiac changes in patients receiving omega-3 fatty acid supplementation. We set out to determine the pro-inflammatory effects of multiple PMs (urban and fine) on pulmonary EC NO bioavailability and protein expression, and whether EPA restores EC function under these conditions.
We pretreated pulmonary ECs with EPA and then exposed them to urban or fine air pollution PMs. LC/MS-based proteomic analysis to assess relative expression levels. Expression of adhesion molecules was measured by immunochemistry. The ratio of NO to peroxynitrite (ONOO–) release, an indication of eNOS coupling, was measured using porphyrinic nanosensors following calcium stimulation. Urban/fine PMs also modulated 9/12 and 13/36 proteins, respectively, linked to platelet and neutrophil degranulation pathways and caused > 50% (p |
| doi_str_mv | 10.1016/j.biopha.2023.114629 |
| format | Article |
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We pretreated pulmonary ECs with EPA and then exposed them to urban or fine air pollution PMs. LC/MS-based proteomic analysis to assess relative expression levels. Expression of adhesion molecules was measured by immunochemistry. The ratio of NO to peroxynitrite (ONOO–) release, an indication of eNOS coupling, was measured using porphyrinic nanosensors following calcium stimulation. Urban/fine PMs also modulated 9/12 and 13/36 proteins, respectively, linked to platelet and neutrophil degranulation pathways and caused > 50% (p < 0.001) decrease in the stimulated NO/ONOO– release ratio. EPA treatment altered expression of proteins involved in these inflammatory pathways, including a decrease in peroxiredoxin-5 and an increase in superoxide dismutase-1. EPA also increased expression of heme oxygenase-1 (HMOX1), a cytoprotective protein, by 2.1-fold (p = 0.024). EPA reduced elevations in sICAM-1 levels by 22% (p < 0.01) and improved the NO/ONOO– release ratio by > 35% (p < 0.05).
These cellular changes may contribute to anti-inflammatory, cytoprotective and lipid changes associated with EPA treatment during air pollution exposure.</description><identifier>ISSN: 0753-3322</identifier><identifier>ISSN: 1950-6007</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2023.114629</identifier><identifier>PMID: 37027984</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Air pollution ; Air Pollution - adverse effects ; Cardiovascular Diseases ; Eicosapentaenoic Acid ; Humans ; Inflammation - chemically induced ; Particulate Matter - adverse effects ; Proteomics ; Pulmonary endothelial function ; Vascular Diseases</subject><ispartof>Biomedicine & pharmacotherapy, 2023-06, Vol.162, p.114629, Article 114629</ispartof><rights>2023 The Authors</rights><rights>Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-d3ff59aba786712f894006abdb526d79a13f971d5f0051a79cdb135d2821712c3</citedby><cites>FETCH-LOGICAL-c408t-d3ff59aba786712f894006abdb526d79a13f971d5f0051a79cdb135d2821712c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0753332223004171$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37027984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sherratt, Samuel C.R.</creatorcontrib><creatorcontrib>Libby, Peter</creatorcontrib><creatorcontrib>Dawoud, Hazem</creatorcontrib><creatorcontrib>Bhatt, Deepak L.</creatorcontrib><creatorcontrib>Malinski, Tadeusz</creatorcontrib><creatorcontrib>Mason, R. Preston</creatorcontrib><title>Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description>Inhalation of air pollution small particle matter (PM) is a leading cause of cardiovascular (CV) disease. Exposure to PMs causes endothelial cell (EC) dysfunction as evidenced by nitric oxide (NO) synthase uncoupling, vasoconstriction and inflammation. Eicosapentaenoic acid (EPA) has been shown to mitigate PM-induced adverse cardiac changes in patients receiving omega-3 fatty acid supplementation. We set out to determine the pro-inflammatory effects of multiple PMs (urban and fine) on pulmonary EC NO bioavailability and protein expression, and whether EPA restores EC function under these conditions.
We pretreated pulmonary ECs with EPA and then exposed them to urban or fine air pollution PMs. LC/MS-based proteomic analysis to assess relative expression levels. Expression of adhesion molecules was measured by immunochemistry. The ratio of NO to peroxynitrite (ONOO–) release, an indication of eNOS coupling, was measured using porphyrinic nanosensors following calcium stimulation. Urban/fine PMs also modulated 9/12 and 13/36 proteins, respectively, linked to platelet and neutrophil degranulation pathways and caused > 50% (p < 0.001) decrease in the stimulated NO/ONOO– release ratio. EPA treatment altered expression of proteins involved in these inflammatory pathways, including a decrease in peroxiredoxin-5 and an increase in superoxide dismutase-1. EPA also increased expression of heme oxygenase-1 (HMOX1), a cytoprotective protein, by 2.1-fold (p = 0.024). EPA reduced elevations in sICAM-1 levels by 22% (p < 0.01) and improved the NO/ONOO– release ratio by > 35% (p < 0.05).
These cellular changes may contribute to anti-inflammatory, cytoprotective and lipid changes associated with EPA treatment during air pollution exposure.</description><subject>Air pollution</subject><subject>Air Pollution - adverse effects</subject><subject>Cardiovascular Diseases</subject><subject>Eicosapentaenoic Acid</subject><subject>Humans</subject><subject>Inflammation - chemically induced</subject><subject>Particulate Matter - adverse effects</subject><subject>Proteomics</subject><subject>Pulmonary endothelial function</subject><subject>Vascular Diseases</subject><issn>0753-3322</issn><issn>1950-6007</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtv1DAUhSMEokPhHyDkZVlk8GMSxxukqhoeUiVYwNpy7JuOR44d_ED0V_EXcZrCktWVrr5zrn1O07wmeE8w6d-d96MNy0ntKaZsT8ihp-JJsyOiw22PMX_a7DDvWMsYpRfNi5TOGOOuZ8Pz5oJxTLkYDrvm99HqkNQCPivwwWqktDXo6vj1-i2KYIqGhJbi5uBVvEfgTcgncFY5ZO7TVLzONnikvEHWT07Ns3pYmAIoB6RPyt9VB-vREkOGOuHXEiGlDYrW362bkEp8ECwqZquLUxlQtcoQkbIRLcG5shq_bJ5NyiV49Tgvm-8fjt9uPrW3Xz5-vrm-bfUBD7k1bJo6oUbFh54TOg3igHGvRjN2tDdcKMImwYnpppoJUVxoMxLWGTpQUnnNLpurzbc--0eBlOVskwbnlIdQklzj45gLLip62FAdQ0oRJrlEO9e0JMFyrUqe5VaVXKuSW1VV9ubxQhlnMP9Ef7upwPsNgPrPnxaiTNqC12BsBJ2lCfb_F_4A4N2rWg</recordid><startdate>202306</startdate><enddate>202306</enddate><creator>Sherratt, Samuel C.R.</creator><creator>Libby, Peter</creator><creator>Dawoud, Hazem</creator><creator>Bhatt, Deepak L.</creator><creator>Malinski, Tadeusz</creator><creator>Mason, R. Preston</creator><general>Elsevier Masson SAS</general><scope>6I.</scope><scope>AAFTH</scope><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>202306</creationdate><title>Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution</title><author>Sherratt, Samuel C.R. ; Libby, Peter ; Dawoud, Hazem ; Bhatt, Deepak L. ; Malinski, Tadeusz ; Mason, R. 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We set out to determine the pro-inflammatory effects of multiple PMs (urban and fine) on pulmonary EC NO bioavailability and protein expression, and whether EPA restores EC function under these conditions.
We pretreated pulmonary ECs with EPA and then exposed them to urban or fine air pollution PMs. LC/MS-based proteomic analysis to assess relative expression levels. Expression of adhesion molecules was measured by immunochemistry. The ratio of NO to peroxynitrite (ONOO–) release, an indication of eNOS coupling, was measured using porphyrinic nanosensors following calcium stimulation. Urban/fine PMs also modulated 9/12 and 13/36 proteins, respectively, linked to platelet and neutrophil degranulation pathways and caused > 50% (p < 0.001) decrease in the stimulated NO/ONOO– release ratio. EPA treatment altered expression of proteins involved in these inflammatory pathways, including a decrease in peroxiredoxin-5 and an increase in superoxide dismutase-1. EPA also increased expression of heme oxygenase-1 (HMOX1), a cytoprotective protein, by 2.1-fold (p = 0.024). EPA reduced elevations in sICAM-1 levels by 22% (p < 0.01) and improved the NO/ONOO– release ratio by > 35% (p < 0.05).
These cellular changes may contribute to anti-inflammatory, cytoprotective and lipid changes associated with EPA treatment during air pollution exposure.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>37027984</pmid><doi>10.1016/j.biopha.2023.114629</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Air pollution Air Pollution - adverse effects Cardiovascular Diseases Eicosapentaenoic Acid Humans Inflammation - chemically induced Particulate Matter - adverse effects Proteomics Pulmonary endothelial function Vascular Diseases |
| title | Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution |
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