Loading…
The environmental carcinogen benzo[a]pyrene induces expression of monocyte-chemoattractant protein-1 in vascular tissue: a possible role in atherogenesis
Exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs) has been implicated in the aetiology of atherosclerosis. Previously we showed that chronic exposure of ApoE-/- mice to the prototype PAH benzo[a]pyrene (B[a]P) causes enhanced progression of atherosclerosis, which was characterised by...
Saved in:
| Published in: | Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis 2007-08, Vol.621 (1-2), p.31-41 |
|---|---|
| Main Authors: | , , , , , , |
| Format: | Article |
| Language: | English |
| Citations: | Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c391t-993cf3e91fde2f6b5f89bbb609eddeff3faf5456bb7d147395eb511d7be86e163 |
|---|---|
| cites | |
| container_end_page | 41 |
| container_issue | 1-2 |
| container_start_page | 31 |
| container_title | Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis |
| container_volume | 621 |
| creator | Knaapen, A M Curfs, D M Pachen, D M Gottschalk, R W de Winther, MPJ Daemen, MJ Van Schooten, FJ |
| description | Exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs) has been implicated in the aetiology of atherosclerosis. Previously we showed that chronic exposure of ApoE-/- mice to the prototype PAH benzo[a]pyrene (B[a]P) causes enhanced progression of atherosclerosis, which was characterised by an increased inflammatory cell content in the atherosclerotic plaques. The aim of the present study was to evaluate the effect of B[a]P on vascular expression of monocyte-chemoattractant protein 1 (MCP-1), which is a crucial molecule promoting the recruitment of monocytes into atherosclerotic lesions. We hypothesised that B[a]P-induced expression of MCP-1 is mediated through aryl hydrocarbon receptor (AhR) activation. Initially we performed in vivo studies showing that acute treatment with B[a]P induces MCP-1 gene expression in aortic tissue of ApoE-/- mice. These observations could be confirmed by in vitro studies with human endothelial cells (RF24 cell line and primary HUVEC), showing a dose- and time-dependent increase in MCP-1 expression upon exposure to B[a]P. This was paralleled by an induction of cytochrome P450 1A1 and 1B1, indicating Ah receptor activation. No increased gene expression (MCP-1, CYP1A1 and 1B1) was found upon incubation with the structural isomer benzo[e]pyrene, which is a weak AhR agonist. Moreover, B[a]P-induced MCP-1 gene and protein expression was inhibited by co-treatment with the AhR antagonist alpha -naphthoflavone. In addition to its effect on basal gene expression, we showed that B[a]P significantly enhanced TNF alpha -induced expression of MCP-1. We were unable to block B[a]P-induced MCP-1 expression by antioxidant treatment. In contrast, we found that addition of N-acetylcysteine or vitamin C enhanced transcription of MCP-1 by B[a]P. In conclusion, our studies revealed potent vascular pro-inflammatory effects of B[a]P, as evidenced by AhR-mediated induction of MCP-1. These observations further contribute to the concept that induction of inflammation is a crucial process in PAH-enhanced atherogenesis. |
| doi_str_mv | 10.1016/j.mrfmmm.2006.12.010 |
| format | article |
| fullrecord | <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_miscellaneous_19732603</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19732603</sourcerecordid><originalsourceid>FETCH-LOGICAL-c391t-993cf3e91fde2f6b5f89bbb609eddeff3faf5456bb7d147395eb511d7be86e163</originalsourceid><addsrcrecordid>eNotzr1OwzAUBWALgUQpvAGDJ7YE3zhxajZU8SdVYikTQpXtXNNUsV1sp6K8CW9LEUxnOt85hFwCK4GBuN6ULlrnXFkxJkqoSgbsiEwYq9qiAdYekwnwmShAivqUnKW0YawWTdVOyPdyjRT9ro_BO_RZDdSoaHof3tFTjf4rvKq37T6iR9r7bjSYKH5uI6bUB0-DpS74YPYZC7NGF1TOUZmsfKbbGDL2voBDke5UMuOgIs19SiPeUEW34WDoAWkMwy9OVV5j_B3G1KdzcmLVkPDiP6fk5f5uOX8sFs8PT_PbRWG4hFxIyY3lKMF2WFmhGzuTWmvBJHYdWsutsk3dCK3bDuqWywZ1A9C1GmcCQfApufpzD3c_Rkx55fpkcBiUxzCmFciWV4Jx_gP5uHMH</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>19732603</pqid></control><display><type>article</type><title>The environmental carcinogen benzo[a]pyrene induces expression of monocyte-chemoattractant protein-1 in vascular tissue: a possible role in atherogenesis</title><source>ScienceDirect Journals</source><creator>Knaapen, A M ; Curfs, D M ; Pachen, D M ; Gottschalk, R W ; de Winther, MPJ ; Daemen, MJ ; Van Schooten, FJ</creator><creatorcontrib>Knaapen, A M ; Curfs, D M ; Pachen, D M ; Gottschalk, R W ; de Winther, MPJ ; Daemen, MJ ; Van Schooten, FJ</creatorcontrib><description>Exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs) has been implicated in the aetiology of atherosclerosis. Previously we showed that chronic exposure of ApoE-/- mice to the prototype PAH benzo[a]pyrene (B[a]P) causes enhanced progression of atherosclerosis, which was characterised by an increased inflammatory cell content in the atherosclerotic plaques. The aim of the present study was to evaluate the effect of B[a]P on vascular expression of monocyte-chemoattractant protein 1 (MCP-1), which is a crucial molecule promoting the recruitment of monocytes into atherosclerotic lesions. We hypothesised that B[a]P-induced expression of MCP-1 is mediated through aryl hydrocarbon receptor (AhR) activation. Initially we performed in vivo studies showing that acute treatment with B[a]P induces MCP-1 gene expression in aortic tissue of ApoE-/- mice. These observations could be confirmed by in vitro studies with human endothelial cells (RF24 cell line and primary HUVEC), showing a dose- and time-dependent increase in MCP-1 expression upon exposure to B[a]P. This was paralleled by an induction of cytochrome P450 1A1 and 1B1, indicating Ah receptor activation. No increased gene expression (MCP-1, CYP1A1 and 1B1) was found upon incubation with the structural isomer benzo[e]pyrene, which is a weak AhR agonist. Moreover, B[a]P-induced MCP-1 gene and protein expression was inhibited by co-treatment with the AhR antagonist alpha -naphthoflavone. In addition to its effect on basal gene expression, we showed that B[a]P significantly enhanced TNF alpha -induced expression of MCP-1. We were unable to block B[a]P-induced MCP-1 expression by antioxidant treatment. In contrast, we found that addition of N-acetylcysteine or vitamin C enhanced transcription of MCP-1 by B[a]P. In conclusion, our studies revealed potent vascular pro-inflammatory effects of B[a]P, as evidenced by AhR-mediated induction of MCP-1. These observations further contribute to the concept that induction of inflammation is a crucial process in PAH-enhanced atherogenesis.</description><identifier>ISSN: 1386-1964</identifier><identifier>EISSN: 0027-5107</identifier><identifier>DOI: 10.1016/j.mrfmmm.2006.12.010</identifier><language>eng</language><ispartof>Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis, 2007-08, Vol.621 (1-2), p.31-41</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-993cf3e91fde2f6b5f89bbb609eddeff3faf5456bb7d147395eb511d7be86e163</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids></links><search><creatorcontrib>Knaapen, A M</creatorcontrib><creatorcontrib>Curfs, D M</creatorcontrib><creatorcontrib>Pachen, D M</creatorcontrib><creatorcontrib>Gottschalk, R W</creatorcontrib><creatorcontrib>de Winther, MPJ</creatorcontrib><creatorcontrib>Daemen, MJ</creatorcontrib><creatorcontrib>Van Schooten, FJ</creatorcontrib><title>The environmental carcinogen benzo[a]pyrene induces expression of monocyte-chemoattractant protein-1 in vascular tissue: a possible role in atherogenesis</title><title>Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis</title><description>Exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs) has been implicated in the aetiology of atherosclerosis. Previously we showed that chronic exposure of ApoE-/- mice to the prototype PAH benzo[a]pyrene (B[a]P) causes enhanced progression of atherosclerosis, which was characterised by an increased inflammatory cell content in the atherosclerotic plaques. The aim of the present study was to evaluate the effect of B[a]P on vascular expression of monocyte-chemoattractant protein 1 (MCP-1), which is a crucial molecule promoting the recruitment of monocytes into atherosclerotic lesions. We hypothesised that B[a]P-induced expression of MCP-1 is mediated through aryl hydrocarbon receptor (AhR) activation. Initially we performed in vivo studies showing that acute treatment with B[a]P induces MCP-1 gene expression in aortic tissue of ApoE-/- mice. These observations could be confirmed by in vitro studies with human endothelial cells (RF24 cell line and primary HUVEC), showing a dose- and time-dependent increase in MCP-1 expression upon exposure to B[a]P. This was paralleled by an induction of cytochrome P450 1A1 and 1B1, indicating Ah receptor activation. No increased gene expression (MCP-1, CYP1A1 and 1B1) was found upon incubation with the structural isomer benzo[e]pyrene, which is a weak AhR agonist. Moreover, B[a]P-induced MCP-1 gene and protein expression was inhibited by co-treatment with the AhR antagonist alpha -naphthoflavone. In addition to its effect on basal gene expression, we showed that B[a]P significantly enhanced TNF alpha -induced expression of MCP-1. We were unable to block B[a]P-induced MCP-1 expression by antioxidant treatment. In contrast, we found that addition of N-acetylcysteine or vitamin C enhanced transcription of MCP-1 by B[a]P. In conclusion, our studies revealed potent vascular pro-inflammatory effects of B[a]P, as evidenced by AhR-mediated induction of MCP-1. These observations further contribute to the concept that induction of inflammation is a crucial process in PAH-enhanced atherogenesis.</description><issn>1386-1964</issn><issn>0027-5107</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNotzr1OwzAUBWALgUQpvAGDJ7YE3zhxajZU8SdVYikTQpXtXNNUsV1sp6K8CW9LEUxnOt85hFwCK4GBuN6ULlrnXFkxJkqoSgbsiEwYq9qiAdYekwnwmShAivqUnKW0YawWTdVOyPdyjRT9ro_BO_RZDdSoaHof3tFTjf4rvKq37T6iR9r7bjSYKH5uI6bUB0-DpS74YPYZC7NGF1TOUZmsfKbbGDL2voBDke5UMuOgIs19SiPeUEW34WDoAWkMwy9OVV5j_B3G1KdzcmLVkPDiP6fk5f5uOX8sFs8PT_PbRWG4hFxIyY3lKMF2WFmhGzuTWmvBJHYdWsutsk3dCK3bDuqWywZ1A9C1GmcCQfApufpzD3c_Rkx55fpkcBiUxzCmFciWV4Jx_gP5uHMH</recordid><startdate>20070801</startdate><enddate>20070801</enddate><creator>Knaapen, A M</creator><creator>Curfs, D M</creator><creator>Pachen, D M</creator><creator>Gottschalk, R W</creator><creator>de Winther, MPJ</creator><creator>Daemen, MJ</creator><creator>Van Schooten, FJ</creator><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20070801</creationdate><title>The environmental carcinogen benzo[a]pyrene induces expression of monocyte-chemoattractant protein-1 in vascular tissue: a possible role in atherogenesis</title><author>Knaapen, A M ; Curfs, D M ; Pachen, D M ; Gottschalk, R W ; de Winther, MPJ ; Daemen, MJ ; Van Schooten, FJ</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-993cf3e91fde2f6b5f89bbb609eddeff3faf5456bb7d147395eb511d7be86e163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Knaapen, A M</creatorcontrib><creatorcontrib>Curfs, D M</creatorcontrib><creatorcontrib>Pachen, D M</creatorcontrib><creatorcontrib>Gottschalk, R W</creatorcontrib><creatorcontrib>de Winther, MPJ</creatorcontrib><creatorcontrib>Daemen, MJ</creatorcontrib><creatorcontrib>Van Schooten, FJ</creatorcontrib><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Knaapen, A M</au><au>Curfs, D M</au><au>Pachen, D M</au><au>Gottschalk, R W</au><au>de Winther, MPJ</au><au>Daemen, MJ</au><au>Van Schooten, FJ</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The environmental carcinogen benzo[a]pyrene induces expression of monocyte-chemoattractant protein-1 in vascular tissue: a possible role in atherogenesis</atitle><jtitle>Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis</jtitle><date>2007-08-01</date><risdate>2007</risdate><volume>621</volume><issue>1-2</issue><spage>31</spage><epage>41</epage><pages>31-41</pages><issn>1386-1964</issn><eissn>0027-5107</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs) has been implicated in the aetiology of atherosclerosis. Previously we showed that chronic exposure of ApoE-/- mice to the prototype PAH benzo[a]pyrene (B[a]P) causes enhanced progression of atherosclerosis, which was characterised by an increased inflammatory cell content in the atherosclerotic plaques. The aim of the present study was to evaluate the effect of B[a]P on vascular expression of monocyte-chemoattractant protein 1 (MCP-1), which is a crucial molecule promoting the recruitment of monocytes into atherosclerotic lesions. We hypothesised that B[a]P-induced expression of MCP-1 is mediated through aryl hydrocarbon receptor (AhR) activation. Initially we performed in vivo studies showing that acute treatment with B[a]P induces MCP-1 gene expression in aortic tissue of ApoE-/- mice. These observations could be confirmed by in vitro studies with human endothelial cells (RF24 cell line and primary HUVEC), showing a dose- and time-dependent increase in MCP-1 expression upon exposure to B[a]P. This was paralleled by an induction of cytochrome P450 1A1 and 1B1, indicating Ah receptor activation. No increased gene expression (MCP-1, CYP1A1 and 1B1) was found upon incubation with the structural isomer benzo[e]pyrene, which is a weak AhR agonist. Moreover, B[a]P-induced MCP-1 gene and protein expression was inhibited by co-treatment with the AhR antagonist alpha -naphthoflavone. In addition to its effect on basal gene expression, we showed that B[a]P significantly enhanced TNF alpha -induced expression of MCP-1. We were unable to block B[a]P-induced MCP-1 expression by antioxidant treatment. In contrast, we found that addition of N-acetylcysteine or vitamin C enhanced transcription of MCP-1 by B[a]P. In conclusion, our studies revealed potent vascular pro-inflammatory effects of B[a]P, as evidenced by AhR-mediated induction of MCP-1. These observations further contribute to the concept that induction of inflammation is a crucial process in PAH-enhanced atherogenesis.</abstract><doi>10.1016/j.mrfmmm.2006.12.010</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1386-1964 |
| ispartof | Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis, 2007-08, Vol.621 (1-2), p.31-41 |
| issn | 1386-1964 0027-5107 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_19732603 |
| source | ScienceDirect Journals |
| title | The environmental carcinogen benzo[a]pyrene induces expression of monocyte-chemoattractant protein-1 in vascular tissue: a possible role in atherogenesis |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-22T16%3A34%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20environmental%20carcinogen%20benzo%5Ba%5Dpyrene%20induces%20expression%20of%20monocyte-chemoattractant%20protein-1%20in%20vascular%20tissue:%20a%20possible%20role%20in%20atherogenesis&rft.jtitle=Mutation%20Research-Fundamental%20and%20Molecular%20Mechanisms%20of%20Mutagenesis&rft.au=Knaapen,%20A%20M&rft.date=2007-08-01&rft.volume=621&rft.issue=1-2&rft.spage=31&rft.epage=41&rft.pages=31-41&rft.issn=1386-1964&rft.eissn=0027-5107&rft_id=info:doi/10.1016/j.mrfmmm.2006.12.010&rft_dat=%3Cproquest%3E19732603%3C/proquest%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c391t-993cf3e91fde2f6b5f89bbb609eddeff3faf5456bb7d147395eb511d7be86e163%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=19732603&rft_id=info:pmid/&rfr_iscdi=true |