Endothelial cell microparticles act as centers of matrix metalloproteinsase‐2 (MMP‐2) activation and vascular matrix remodeling
Identifieur interne : 003146 ( Istex/Corpus ); précédent : 003145; suivant : 003147Endothelial cell microparticles act as centers of matrix metalloproteinsase‐2 (MMP‐2) activation and vascular matrix remodeling
Auteurs : Thomas P. Lozito ; Rocky S. TuanSource :
- Journal of Cellular Physiology [ 0021-9541 ] ; 2012-02.
English descriptors
- KwdEn :
- Abcam, Activity assays, Apma, Apoptotic bodies, Assay, Avidin, Bind exogenous, Binding interactions, Biotin, Bronectin, Bronectin receptor, Bronectin receptors, Cellular, Cellular physiology, Combes, Control conditions, Culture conditions, Cytokine, Diamant, Edta, Elisa, Endogenous, Endothelial, Endothelial cells, Endothelial microparticles, Exogenous, Exogenous mmps, Extracellular, Extracellular matrix molecules, Gelatin, Gelatin zymography, High levels, Higher levels, Hypoxia, Hypoxic conditions, Inhibitor, Inhibitor assays, Integrin, Integrin avb3, Lozito, Matrix, Matrix metalloproteinases, Matrix molecules, Membrane, Membrane extracts, Metalloproteinases, Microec, Microec membrane extracts, Microecs, Microparticles, Mmmp, Mmmp results, Mmps, Monomeric avidin, Msc, Pathological conditions, Pellet, Perivascular, Perivascular niche, Photometry, Physiology, Protein samples, Receptor, Room temperature, Santa cruz, Substrate protein, Timps, Tuan, Ultracentrifugation pellets, Uorescence, Uorescence photometry, Uorescence scans, Uorescent, Vascular matrix, Vehicle control, Vehicle controls, Vesicle, Western blot, Western blot analysis, Western blots, Zymography.
- Teeft :
- Abcam, Activity assays, Apma, Apoptotic bodies, Assay, Avidin, Bind exogenous, Binding interactions, Biotin, Bronectin, Bronectin receptor, Bronectin receptors, Cellular, Cellular physiology, Combes, Control conditions, Culture conditions, Cytokine, Diamant, Edta, Elisa, Endogenous, Endothelial, Endothelial cells, Endothelial microparticles, Exogenous, Exogenous mmps, Extracellular, Extracellular matrix molecules, Gelatin, Gelatin zymography, High levels, Higher levels, Hypoxia, Hypoxic conditions, Inhibitor, Inhibitor assays, Integrin, Integrin avb3, Lozito, Matrix, Matrix metalloproteinases, Matrix molecules, Membrane, Membrane extracts, Metalloproteinases, Microec, Microec membrane extracts, Microecs, Microparticles, Mmmp, Mmmp results, Mmps, Monomeric avidin, Msc, Pathological conditions, Pellet, Perivascular, Perivascular niche, Photometry, Physiology, Protein samples, Receptor, Room temperature, Santa cruz, Substrate protein, Timps, Tuan, Ultracentrifugation pellets, Uorescence, Uorescence photometry, Uorescence scans, Uorescent, Vascular matrix, Vehicle control, Vehicle controls, Vesicle, Western blot, Western blot analysis, Western blots, Zymography.
Abstract
Endothelial cell (EC)‐derived microparticles (MPs) are small membrane vesicles associated with various vascular pathologies. Here, we investigated the role of MPs in matrix remodeling by analyzing their interactions with the extracellular matrix. MPs were shown to bind preferentially to surfaces coated with matrix molecules, and MPs bound fibronectin via integrin αV. MPs isolated from EC‐conditioned medium (Sup) were significantly enriched for matrix‐altering proteases, including matrix metalloproteinases (MMPs). MPs lacked the MMP inhibitors TIMP‐1 and TIMP‐2 found in the Sup and, while Sup strongly inhibited MMP activities but MPs did not. In fact, MPs were shown to bind and activate both endogenous and exogenous proMMP‐2. Taken together, these results indicate that MPs interact with extracellular matrices, where they localize and activate MMP‐2 to modify the surrounding matrix molecules. These findings provide insights into the cellular mechanisms of vascular matrix remodeling and identify new targets of vascular pathologies. J. Cell. Physiol. 227: 534–549, 2012. © 2011 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/jcp.22744
Links to Exploration step
ISTEX:CF56B77A871A61746F3030E019436D730DBABE37Le document en format XML
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type="abstract" xml:lang="en">Endothelial cell (EC)‐derived microparticles (MPs) are small membrane vesicles associated with various vascular pathologies. 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Tuan</name><affiliations><json:string>Cartilage Biology and Orthopaedics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland</json:string><json:string>Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</json:string><json:string>E-mail: rst13@pitt.edu</json:string><json:string>Correspondence address: Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, 450 Technology Drive, Room 221, Pittsburgh, PA 15219.</json:string></affiliations></json:item></author><articleId><json:string>JCP22744</json:string></articleId><arkIstex>ark:/67375/WNG-5RL2F839-R</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Endothelial cell (EC)‐derived microparticles (MPs) are small membrane vesicles associated with various vascular pathologies. Here, we investigated the role of MPs in matrix remodeling by analyzing their interactions with the extracellular matrix. MPs were shown to bind preferentially to surfaces coated with matrix molecules, and MPs bound fibronectin via integrin αV. MPs isolated from EC‐conditioned medium (Sup) were significantly enriched for matrix‐altering proteases, including matrix metalloproteinases (MMPs). MPs lacked the MMP inhibitors TIMP‐1 and TIMP‐2 found in the Sup and, while Sup strongly inhibited MMP activities but MPs did not. In fact, MPs were shown to bind and activate both endogenous and exogenous proMMP‐2. Taken together, these results indicate that MPs interact with extracellular matrices, where they localize and activate MMP‐2 to modify the surrounding matrix molecules. These findings provide insights into the cellular mechanisms of vascular matrix remodeling and identify new targets of vascular pathologies. J. Cell. Physiol. 227: 534–549, 2012. © 2011 Wiley Periodicals, Inc.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>157</abstractWordCount><abstractCharCount>1113</abstractCharCount><keywordCount>0</keywordCount><score>8.884</score><pdfWordCount>8111</pdfWordCount><pdfCharCount>51058</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>16</pdfPageCount><pdfPageSize>592 x 789 pts</pdfPageSize></qualityIndicators><title>Endothelial cell microparticles act as centers of matrix metalloproteinsase‐2 (MMP‐2) activation and vascular matrix remodeling</title><pmid><json:string>21437907</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Cellular Physiology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1097-4652</json:string></doi><issn><json:string>0021-9541</json:string></issn><eissn><json:string>1097-4652</json:string></eissn><publisherId><json:string>JCP</json:string></publisherId><volume>227</volume><issue>2</issue><pages><first>534</first><last>549</last><total>16</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Original Research Article</value></json:item></subject></host><namedEntities><unitex><date><json:string>2012</json:string></date><geogName></geogName><orgName><json:string>National Institutes of Health, Department of Health and Human Services</json:string><json:string>Santa Cruz Biotechnology, Inc.</json:string><json:string>Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Endothelial</json:string><json:string>National Institute of Arthritis</json:string><json:string>Department of Orthopaedic Surgery</json:string><json:string>Biochem</json:string><json:string>D Systems, Minneapolis</json:string><json:string>Tuan, Center for Cellular and Molecular Engineering</json:string><json:string>Beckman Coulter, Inc.</json:string><json:string>Calbiochem</json:string><json:string>Wiley Periodicals, Inc</json:string><json:string>University of Washington</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Lawley</json:string><json:string>Candal</json:string><json:string>Abid Hussein</json:string><json:string>T. 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remodeling</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><licence>Copyright © 2011 Wiley Periodicals, Inc.</licence></availability><date type="published" when="2012-02"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main" xml:lang="en">Endothelial cell microparticles act as centers of matrix metalloproteinsase‐2 (MMP‐2) activation and vascular matrix remodeling</title><title level="a" type="short" xml:lang="en">ENDOTHELIAL MICROPARTICLES AND ECM REMODELING</title><author xml:id="author-0000"><persName><forename type="first">Thomas P.</forename><surname>Lozito</surname></persName><affiliation>Cartilage Biology and Orthopaedics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland<address><country key="US"></country></address></affiliation><affiliation>Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania<address><country key="US"></country></address></affiliation></author><author xml:id="author-0001" role="corresp"><persName><forename type="first">Rocky S.</forename><surname>Tuan</surname></persName><email>rst13@pitt.edu</email><affiliation>Cartilage Biology and Orthopaedics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland<address><country key="US"></country></address></affiliation><affiliation>Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania<address><country key="US"></country></address></affiliation><affiliation>Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, 450 Technology Drive, Room 221, Pittsburgh, PA 15219.</affiliation></author><idno type="istex">CF56B77A871A61746F3030E019436D730DBABE37</idno><idno type="ark">ark:/67375/WNG-5RL2F839-R</idno><idno type="DOI">10.1002/jcp.22744</idno><idno type="unit">JCP22744</idno><idno type="toTypesetVersion">file:JCP.JCP22744.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Cellular Physiology</title><title level="j" type="alt">JOURNAL OF CELLULAR PHYSIOLOGY</title><idno type="pISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><idno type="book-DOI">10.1002/(ISSN)1097-4652</idno><idno type="book-part-DOI">10.1002/jcp.v227.2</idno><idno type="product">JCP</idno><imprint><biblScope unit="vol">227</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="534">534</biblScope><biblScope unit="page" to="549">549</biblScope><biblScope unit="page-count">16</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2012-02"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>Endothelial cell (EC)‐derived microparticles (MPs) are small membrane vesicles associated with various vascular pathologies. Here, we investigated the role of MPs in matrix remodeling by analyzing their interactions with the extracellular matrix. MPs were shown to bind preferentially to surfaces coated with matrix molecules, and MPs bound fibronectin via integrin α<hi rend="subscript">V</hi>. MPs isolated from EC‐conditioned medium (Sup) were significantly enriched for matrix‐altering proteases, including matrix metalloproteinases (MMPs). MPs lacked the MMP inhibitors TIMP‐1 and TIMP‐2 found in the Sup and, while Sup strongly inhibited MMP activities but MPs did not. In fact, MPs were shown to bind and activate both endogenous and exogenous proMMP‐2. Taken together, these results indicate that MPs interact with extracellular matrices, where they localize and activate MMP‐2 to modify the surrounding matrix molecules. These findings provide insights into the cellular mechanisms of vascular matrix remodeling and identify new targets of vascular pathologies. J. Cell. Physiol. 227: 534–549, 2012. © 2011 Wiley Periodicals, Inc.</p></abstract><textClass><keywords rend="articleCategory"><term>Original Research Article</term></keywords><keywords rend="tocHeading1"><term>Original Research Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/CF56B77A871A61746F3030E019436D730DBABE37/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4652</doi><issn type="print">0021-9541</issn><issn type="electronic">1097-4652</issn><idGroup><id type="product" value="JCP"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF CELLULAR PHYSIOLOGY">Journal of Cellular Physiology</title><title type="short">J. Cell. Physiol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="20"><doi origin="wiley" registered="yes">10.1002/jcp.v227.2</doi><numberingGroup><numbering type="journalVolume" number="227">227</numbering><numbering type="journalIssue">2</numbering></numberingGroup><coverDate startDate="2012-02">February 2012</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="160" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jcp.22744</doi><idGroup><id type="unit" value="JCP22744"></id></idGroup><countGroup><count type="pageTotal" number="16"></count></countGroup><titleGroup><title type="articleCategory">Original Research Article</title><title type="tocHeading1">Original Research Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2011 Wiley Periodicals, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2011-03-14"></event><event type="manuscriptAccepted" date="2011-03-15"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.0.1 mode:FullText" date="2011-12-08"></event><event type="publishedOnlineAccepted" date="2011-03-24"></event><event type="publishedOnlineFinalForm" date="2011-11-23"></event><event type="firstOnline" date="2011-11-23"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-30"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.3.4 mode:FullText" date="2015-02-24"></event></eventGroup><numberingGroup><numbering type="pageFirst">534</numbering><numbering type="pageLast">549</numbering></numberingGroup><correspondenceTo>Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, 450 Technology Drive, Room 221, Pittsburgh, PA 15219.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCP.JCP22744.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="10"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="33"></count><count type="wordTotal" number="8573"></count></countGroup><titleGroup><title type="main" xml:lang="en">Endothelial cell microparticles act as centers of matrix metalloproteinsase‐2 (MMP‐2) activation and vascular matrix remodeling</title><title type="short" xml:lang="en">ENDOTHELIAL MICROPARTICLES AND ECM REMODELING</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Thomas P.</givenNames><familyName>Lozito</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Rocky S.</givenNames><familyName>Tuan</familyName></personName><contactDetails><email>rst13@pitt.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Cartilage Biology and Orthopaedics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>NIAMS IRP</fundingAgency><fundingNumber>Z01AR41131</fundingNumber></fundingInfo><supportingInformation><p>
Supporting information may be found in the online version of this article.
</p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:00219541:media:jcp22744:jcp_22744_sm_SuppMat"></mediaResource><caption>Supplementary Material</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Endothelial cell (EC)‐derived microparticles (MPs) are small membrane vesicles associated with various vascular pathologies. Here, we investigated the role of MPs in matrix remodeling by analyzing their interactions with the extracellular matrix. MPs were shown to bind preferentially to surfaces coated with matrix molecules, and MPs bound fibronectin via integrin α<sub>V</sub>. MPs isolated from EC‐conditioned medium (Sup) were significantly enriched for matrix‐altering proteases, including matrix metalloproteinases (MMPs). MPs lacked the MMP inhibitors TIMP‐1 and TIMP‐2 found in the Sup and, while Sup strongly inhibited MMP activities but MPs did not. In fact, MPs were shown to bind and activate both endogenous and exogenous proMMP‐2. Taken together, these results indicate that MPs interact with extracellular matrices, where they localize and activate MMP‐2 to modify the surrounding matrix molecules. These findings provide insights into the cellular mechanisms of vascular matrix remodeling and identify new targets of vascular pathologies. J. Cell. Physiol. 227: 534–549, 2012. © 2011 Wiley Periodicals, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Endothelial cell microparticles act as centers of matrix metalloproteinsase‐2 (MMP‐2) activation and vascular matrix remodeling</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>ENDOTHELIAL MICROPARTICLES AND ECM REMODELING</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Endothelial cell microparticles act as centers of matrix metalloproteinsase‐2 (MMP‐2) activation and vascular matrix remodeling</title></titleInfo><name type="personal"><namePart type="given">Thomas P.</namePart><namePart type="family">Lozito</namePart><affiliation>Cartilage Biology and Orthopaedics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland</affiliation><affiliation>Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rocky S.</namePart><namePart type="family">Tuan</namePart><affiliation>Cartilage Biology and Orthopaedics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland</affiliation><affiliation>Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania</affiliation><affiliation>E-mail: rst13@pitt.edu</affiliation><affiliation>Correspondence address: Center for Cellular and Molecular Engineering, Department of Orthopaedic Surgery, 450 Technology Drive, Room 221, Pittsburgh, PA 15219.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2012-02</dateIssued><dateCaptured encoding="w3cdtf">2011-03-14</dateCaptured><dateValid encoding="w3cdtf">2011-03-15</dateValid><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">10</extent><extent unit="tables">0</extent><extent unit="references">33</extent><extent unit="words">8573</extent></physicalDescription><abstract lang="en">Endothelial cell (EC)‐derived microparticles (MPs) are small membrane vesicles associated with various vascular pathologies. Here, we investigated the role of MPs in matrix remodeling by analyzing their interactions with the extracellular matrix. MPs were shown to bind preferentially to surfaces coated with matrix molecules, and MPs bound fibronectin via integrin αV. MPs isolated from EC‐conditioned medium (Sup) were significantly enriched for matrix‐altering proteases, including matrix metalloproteinases (MMPs). MPs lacked the MMP inhibitors TIMP‐1 and TIMP‐2 found in the Sup and, while Sup strongly inhibited MMP activities but MPs did not. In fact, MPs were shown to bind and activate both endogenous and exogenous proMMP‐2. Taken together, these results indicate that MPs interact with extracellular matrices, where they localize and activate MMP‐2 to modify the surrounding matrix molecules. These findings provide insights into the cellular mechanisms of vascular matrix remodeling and identify new targets of vascular pathologies. J. Cell. 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