Microparticles from patients with metabolic syndrome induce vascular hypo-reactivity via Fas/Fas-ligand pathway in mice
Microparticles are membrane vesicles with pro-inflammatory properties. Circulating levels of microparticles have previously been found to be elevated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the effects of in vivo treatment with microparticles, from patients wi...
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| Veröffentlicht in: | PloS one 2011-11, Vol.6 (11), p.e27809-e27809 |
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| creator | Agouni, Abdelali Ducluzeau, Pierre-Henri Benameur, Tarek Faure, Sébastien Sladkova, Martina Duluc, Lucie Leftheriotis, Georges Pechanova, Olga Delibegovic, Mirela Martinez, Maria Carmen Andriantsitohaina, Ramaroson |
| description | Microparticles are membrane vesicles with pro-inflammatory properties. Circulating levels of microparticles have previously been found to be elevated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the effects of in vivo treatment with microparticles, from patients with MetS and from healthy subjects (HS), on ex vivo vascular function in mice. Microparticles isolated from MetS patients or HS, or a vehicle were intravenously injected into mice, following which vascular reactivity in response to vasoconstrictor agonists was assessed by myography with respect to cyclo-oxygenase pathway, oxidative and nitrosative stress. Injection of microparticles from MetS patients into mice induced vascular hypo-reactivity in response to serotonin. Hypo-reactivity was associated with up-regulation of inducible NO-synthase and increased production of NO, and was reversed by the NO-synthase inhibitor (N(G)-nitro-L-arginine). The selective COX-2 inhibitor (NS398) reduced the contractile effect of serotonin in aortas from mice treated with vehicle or HS microparticles; however, this was not observed within mice treated with MetS microparticles, probably due to the ability of MetS microparticles to enhance prostacyclin. MetS microparticle-mediated vascular dysfunction was associated with increased reactive oxygen species (ROS) and enhanced expression of the NADPH oxidase subunits. Neutralization of the pro-inflammatory pathway Fas/FasL completely prevented vascular hypo-reactivity and the ability of MetS microparticles to enhance both inducible NO-synthase and monocyte chemoattractant protein-1 (MCP-1). Our data provide evidence that microparticles from MetS patients induce ex vivo vascular dysfunction by increasing both ROS and NO release and by altering cyclo-oxygenase metabolites and MCP-1 through the Fas/FasL pathway. |
| doi_str_mv | 10.1371/journal.pone.0027809 |
| format | Article |
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Circulating levels of microparticles have previously been found to be elevated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the effects of in vivo treatment with microparticles, from patients with MetS and from healthy subjects (HS), on ex vivo vascular function in mice. Microparticles isolated from MetS patients or HS, or a vehicle were intravenously injected into mice, following which vascular reactivity in response to vasoconstrictor agonists was assessed by myography with respect to cyclo-oxygenase pathway, oxidative and nitrosative stress. Injection of microparticles from MetS patients into mice induced vascular hypo-reactivity in response to serotonin. Hypo-reactivity was associated with up-regulation of inducible NO-synthase and increased production of NO, and was reversed by the NO-synthase inhibitor (N(G)-nitro-L-arginine). The selective COX-2 inhibitor (NS398) reduced the contractile effect of serotonin in aortas from mice treated with vehicle or HS microparticles; however, this was not observed within mice treated with MetS microparticles, probably due to the ability of MetS microparticles to enhance prostacyclin. MetS microparticle-mediated vascular dysfunction was associated with increased reactive oxygen species (ROS) and enhanced expression of the NADPH oxidase subunits. Neutralization of the pro-inflammatory pathway Fas/FasL completely prevented vascular hypo-reactivity and the ability of MetS microparticles to enhance both inducible NO-synthase and monocyte chemoattractant protein-1 (MCP-1). Our data provide evidence that microparticles from MetS patients induce ex vivo vascular dysfunction by increasing both ROS and NO release and by altering cyclo-oxygenase metabolites and MCP-1 through the Fas/FasL pathway.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0027809</identifier><identifier>PMID: 22110764</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Angiogenesis ; Animals ; Aorta - cytology ; Aorta - metabolism ; Apoptosis ; Arginine ; Atherosclerosis ; Biology ; Blood platelets ; Cardiovascular disease ; Cell-Derived Microparticles - metabolism ; Chemokine CCL2 - genetics ; Chemokine CCL2 - metabolism ; Contractility ; COX-2 inhibitors ; Cyclooxygenase 2 - metabolism ; Cyclooxygenase-2 ; Cytokines ; Diabetes ; Environmental science ; Ethics ; Fas Ligand Protein - metabolism ; fas Receptor - metabolism ; FasL protein ; Female ; Gene Expression Regulation, Enzymologic ; Health care ; Humans ; Hypertension ; In vivo methods and tests ; Inflammation ; Kinases ; Laboratory animals ; Ligands ; Male ; Medical research ; Medicine ; Membrane vesicles ; Metabolic disorders ; Metabolic syndrome ; Metabolic Syndrome - pathology ; Metabolites ; Mice ; Microparticles ; Middle Aged ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; NAD(P)H oxidase ; NADPH Oxidases - metabolism ; Neutralization ; Nitric oxide ; Nitric Oxide - metabolism ; Oxygen ; Oxygenase ; Pathogenesis ; Patients ; Prostacyclin ; Prostaglandin endoperoxide synthase ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reactivity ; Rodents ; Serotonin ; Signal Transduction ; Smooth muscle ; Thrombosis</subject><ispartof>PloS one, 2011-11, Vol.6 (11), p.e27809-e27809</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Agouni et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Agouni et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-b77d713a5ada2723c8aed64d6dfcd10779f24aa4e07786f217bda02d899f5bc33</citedby><cites>FETCH-LOGICAL-c691t-b77d713a5ada2723c8aed64d6dfcd10779f24aa4e07786f217bda02d899f5bc33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3217000/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3217000/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22110764$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Reitsma, Pieter H.</contributor><creatorcontrib>Agouni, Abdelali</creatorcontrib><creatorcontrib>Ducluzeau, Pierre-Henri</creatorcontrib><creatorcontrib>Benameur, Tarek</creatorcontrib><creatorcontrib>Faure, Sébastien</creatorcontrib><creatorcontrib>Sladkova, Martina</creatorcontrib><creatorcontrib>Duluc, Lucie</creatorcontrib><creatorcontrib>Leftheriotis, Georges</creatorcontrib><creatorcontrib>Pechanova, Olga</creatorcontrib><creatorcontrib>Delibegovic, Mirela</creatorcontrib><creatorcontrib>Martinez, Maria Carmen</creatorcontrib><creatorcontrib>Andriantsitohaina, Ramaroson</creatorcontrib><title>Microparticles from patients with metabolic syndrome induce vascular hypo-reactivity via Fas/Fas-ligand pathway in mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Microparticles are membrane vesicles with pro-inflammatory properties. Circulating levels of microparticles have previously been found to be elevated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the effects of in vivo treatment with microparticles, from patients with MetS and from healthy subjects (HS), on ex vivo vascular function in mice. Microparticles isolated from MetS patients or HS, or a vehicle were intravenously injected into mice, following which vascular reactivity in response to vasoconstrictor agonists was assessed by myography with respect to cyclo-oxygenase pathway, oxidative and nitrosative stress. Injection of microparticles from MetS patients into mice induced vascular hypo-reactivity in response to serotonin. Hypo-reactivity was associated with up-regulation of inducible NO-synthase and increased production of NO, and was reversed by the NO-synthase inhibitor (N(G)-nitro-L-arginine). The selective COX-2 inhibitor (NS398) reduced the contractile effect of serotonin in aortas from mice treated with vehicle or HS microparticles; however, this was not observed within mice treated with MetS microparticles, probably due to the ability of MetS microparticles to enhance prostacyclin. MetS microparticle-mediated vascular dysfunction was associated with increased reactive oxygen species (ROS) and enhanced expression of the NADPH oxidase subunits. Neutralization of the pro-inflammatory pathway Fas/FasL completely prevented vascular hypo-reactivity and the ability of MetS microparticles to enhance both inducible NO-synthase and monocyte chemoattractant protein-1 (MCP-1). Our data provide evidence that microparticles from MetS patients induce ex vivo vascular dysfunction by increasing both ROS and NO release and by altering cyclo-oxygenase metabolites and MCP-1 through the Fas/FasL pathway.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Aorta - cytology</subject><subject>Aorta - metabolism</subject><subject>Apoptosis</subject><subject>Arginine</subject><subject>Atherosclerosis</subject><subject>Biology</subject><subject>Blood platelets</subject><subject>Cardiovascular disease</subject><subject>Cell-Derived Microparticles - metabolism</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Contractility</subject><subject>COX-2 inhibitors</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Cyclooxygenase-2</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Environmental science</subject><subject>Ethics</subject><subject>Fas Ligand Protein - metabolism</subject><subject>fas Receptor - metabolism</subject><subject>FasL protein</subject><subject>Female</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Health care</subject><subject>Humans</subject><subject>Hypertension</subject><subject>In vivo methods and tests</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Ligands</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Membrane vesicles</subject><subject>Metabolic disorders</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - pathology</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Microparticles</subject><subject>Middle Aged</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>NAD(P)H oxidase</subject><subject>NADPH Oxidases - metabolism</subject><subject>Neutralization</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Oxygen</subject><subject>Oxygenase</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Prostacyclin</subject><subject>Prostaglandin endoperoxide synthase</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reactivity</subject><subject>Rodents</subject><subject>Serotonin</subject><subject>Signal Transduction</subject><subject>Smooth muscle</subject><subject>Thrombosis</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7rr6D0QLguJFZ_PRj_RGWBZXB1YW_LoNp0k6zZI2tUlnnH9v6nSXqeyFhJCQPOfNyZucKHqJ0QrTAp_f2nHowKx626kVQqRgqHwUneKSkiQniD4-mp9Ez5y7RSijLM-fRieEYIyKPD2Ndl-0GGwPg9fCKBfXg23jHrxWnXfxTvsmbpWHyhotYrfvZNhXse7kKFS8BSdGA0Pc7HubDAqE11vt9_FWQ3wF7jz0xOgNdHLSbHawD6Fxq4V6Hj2pwTj1Yh7Poh9XH79ffk6ubz6tLy-uE5GX2CdVUcgCU8hAAikIFQyUzFOZy1rIcIWirEkKkKowZXlNcFFJQESysqyzSlB6Fr0-6PbGOj575jimmKA0Q1kRiPWBkBZueT_oFoY9t6D53wU7bPjsDpdKslziCteEpohhVmNWobIkuGaMlixofZhPG6tWSRFMHMAsRJc7nW74xm45DZkjhILAu1lgsL9G5TxvtRPKGOiUHR0vUVbmKU6ntN_8Qz58uZnaQMhfd7UNx4pJk1-kRc5yUhZT2qsHqNCkCm8V_letw_oi4P0iIDBe_fYbGJ3j629f_5-9-blk3x6xjQLjG2fN6LXt3BJMD2D4vM4Nqr73GCM-lcedG3wqDz6XRwh7dfw-90F39UD_APyCDDo</recordid><startdate>20111115</startdate><enddate>20111115</enddate><creator>Agouni, Abdelali</creator><creator>Ducluzeau, Pierre-Henri</creator><creator>Benameur, Tarek</creator><creator>Faure, Sébastien</creator><creator>Sladkova, Martina</creator><creator>Duluc, Lucie</creator><creator>Leftheriotis, Georges</creator><creator>Pechanova, Olga</creator><creator>Delibegovic, Mirela</creator><creator>Martinez, Maria Carmen</creator><creator>Andriantsitohaina, Ramaroson</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20111115</creationdate><title>Microparticles from patients with metabolic syndrome induce vascular hypo-reactivity via Fas/Fas-ligand pathway in mice</title><author>Agouni, Abdelali ; Ducluzeau, Pierre-Henri ; Benameur, Tarek ; Faure, Sébastien ; Sladkova, Martina ; Duluc, Lucie ; Leftheriotis, Georges ; Pechanova, Olga ; Delibegovic, Mirela ; Martinez, Maria Carmen ; Andriantsitohaina, Ramaroson</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-b77d713a5ada2723c8aed64d6dfcd10779f24aa4e07786f217bda02d899f5bc33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Aorta - 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pathology</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Microparticles</topic><topic>Middle Aged</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>NAD(P)H oxidase</topic><topic>NADPH Oxidases - metabolism</topic><topic>Neutralization</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Oxygen</topic><topic>Oxygenase</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Prostacyclin</topic><topic>Prostaglandin endoperoxide synthase</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Reactivity</topic><topic>Rodents</topic><topic>Serotonin</topic><topic>Signal Transduction</topic><topic>Smooth muscle</topic><topic>Thrombosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Agouni, Abdelali</creatorcontrib><creatorcontrib>Ducluzeau, Pierre-Henri</creatorcontrib><creatorcontrib>Benameur, Tarek</creatorcontrib><creatorcontrib>Faure, Sébastien</creatorcontrib><creatorcontrib>Sladkova, Martina</creatorcontrib><creatorcontrib>Duluc, Lucie</creatorcontrib><creatorcontrib>Leftheriotis, Georges</creatorcontrib><creatorcontrib>Pechanova, Olga</creatorcontrib><creatorcontrib>Delibegovic, Mirela</creatorcontrib><creatorcontrib>Martinez, Maria Carmen</creatorcontrib><creatorcontrib>Andriantsitohaina, Ramaroson</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Agouni, Abdelali</au><au>Ducluzeau, Pierre-Henri</au><au>Benameur, Tarek</au><au>Faure, Sébastien</au><au>Sladkova, Martina</au><au>Duluc, Lucie</au><au>Leftheriotis, Georges</au><au>Pechanova, Olga</au><au>Delibegovic, Mirela</au><au>Martinez, Maria Carmen</au><au>Andriantsitohaina, Ramaroson</au><au>Reitsma, Pieter H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microparticles from patients with metabolic syndrome induce vascular hypo-reactivity via Fas/Fas-ligand pathway in mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-11-15</date><risdate>2011</risdate><volume>6</volume><issue>11</issue><spage>e27809</spage><epage>e27809</epage><pages>e27809-e27809</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Microparticles are membrane vesicles with pro-inflammatory properties. Circulating levels of microparticles have previously been found to be elevated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the effects of in vivo treatment with microparticles, from patients with MetS and from healthy subjects (HS), on ex vivo vascular function in mice. Microparticles isolated from MetS patients or HS, or a vehicle were intravenously injected into mice, following which vascular reactivity in response to vasoconstrictor agonists was assessed by myography with respect to cyclo-oxygenase pathway, oxidative and nitrosative stress. Injection of microparticles from MetS patients into mice induced vascular hypo-reactivity in response to serotonin. Hypo-reactivity was associated with up-regulation of inducible NO-synthase and increased production of NO, and was reversed by the NO-synthase inhibitor (N(G)-nitro-L-arginine). The selective COX-2 inhibitor (NS398) reduced the contractile effect of serotonin in aortas from mice treated with vehicle or HS microparticles; however, this was not observed within mice treated with MetS microparticles, probably due to the ability of MetS microparticles to enhance prostacyclin. MetS microparticle-mediated vascular dysfunction was associated with increased reactive oxygen species (ROS) and enhanced expression of the NADPH oxidase subunits. Neutralization of the pro-inflammatory pathway Fas/FasL completely prevented vascular hypo-reactivity and the ability of MetS microparticles to enhance both inducible NO-synthase and monocyte chemoattractant protein-1 (MCP-1). Our data provide evidence that microparticles from MetS patients induce ex vivo vascular dysfunction by increasing both ROS and NO release and by altering cyclo-oxygenase metabolites and MCP-1 through the Fas/FasL pathway.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22110764</pmid><doi>10.1371/journal.pone.0027809</doi><tpages>e27809</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2011-11, Vol.6 (11), p.e27809-e27809 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1312045057 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Angiogenesis Animals Aorta - cytology Aorta - metabolism Apoptosis Arginine Atherosclerosis Biology Blood platelets Cardiovascular disease Cell-Derived Microparticles - metabolism Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Contractility COX-2 inhibitors Cyclooxygenase 2 - metabolism Cyclooxygenase-2 Cytokines Diabetes Environmental science Ethics Fas Ligand Protein - metabolism fas Receptor - metabolism FasL protein Female Gene Expression Regulation, Enzymologic Health care Humans Hypertension In vivo methods and tests Inflammation Kinases Laboratory animals Ligands Male Medical research Medicine Membrane vesicles Metabolic disorders Metabolic syndrome Metabolic Syndrome - pathology Metabolites Mice Microparticles Middle Aged Monocyte chemoattractant protein Monocyte chemoattractant protein 1 NAD(P)H oxidase NADPH Oxidases - metabolism Neutralization Nitric oxide Nitric Oxide - metabolism Oxygen Oxygenase Pathogenesis Patients Prostacyclin Prostaglandin endoperoxide synthase Reactive oxygen species Reactive Oxygen Species - metabolism Reactivity Rodents Serotonin Signal Transduction Smooth muscle Thrombosis |
| title | Microparticles from patients with metabolic syndrome induce vascular hypo-reactivity via Fas/Fas-ligand pathway in mice |
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