Matrix Metalloproteinase-2 and −9 Differentially Regulate Smooth Muscle Cell Migration and Cell-Mediated Collagen Organization
OBJECTIVES—Smooth muscle cells (SMCs) produce both matrix metalloproteinase (MMP)-2 and MMP-9, enzymes with similar in vitro matrix degrading abilities. We compared the specific contributions of these enzymes to SMC-matrix interactions in vitro and in vivo. METHODS AND RESULTS—Using genetic models o...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2004-01, Vol.24 (1), p.54-60 |
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| creator | Johnson, Chad Galis, Zorina S |
| description | OBJECTIVES—Smooth muscle cells (SMCs) produce both matrix metalloproteinase (MMP)-2 and MMP-9, enzymes with similar in vitro matrix degrading abilities. We compared the specific contributions of these enzymes to SMC-matrix interactions in vitro and in vivo.
METHODS AND RESULTS—Using genetic models of deficiency, we investigated MMP-2 and MMP-9 roles in SMC migration in vivo in the formation of intimal hyperplasia and in vitro. In addition, we investigated potential effects of MMP-2 and MMP-9 genetic deficiency on compaction and assembly of collagen by SMCs.
CONCLUSIONS—MMP-2 and MMP-9 genetic deficiency decreased by 81% and 65%, respectively (P |
| doi_str_mv | 10.1161/01.ATV.0000100402.69997.C3 |
| format | Article |
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METHODS AND RESULTS—Using genetic models of deficiency, we investigated MMP-2 and MMP-9 roles in SMC migration in vivo in the formation of intimal hyperplasia and in vitro. In addition, we investigated potential effects of MMP-2 and MMP-9 genetic deficiency on compaction and assembly of collagen by SMCs.
CONCLUSIONS—MMP-2 and MMP-9 genetic deficiency decreased by 81% and 65%, respectively (P <0.01), SMC invasion in vitro and decreased formation of intimal hyperplasia in vivo (P <0.01). However, we found that MMP-9, but not MMP-2, was necessary for organization of collagen by SMCs. Likewise, we found that MMP-9 deficiency resulted in a 50% reduction of SMC attachment to gelatin (P <0.01), indicating that SMCs may use MMP-9 as a bridge between the cell surface and matrix. Furthermore, we found that the hyaluronan receptor, CD44, assists in attachment and utilization of MMP-9 by SMCs. Understanding the specific roles of these MMPs, generally thought to be similar, could improve the design of therapeutic interventions aimed at controlling vascular remodeling.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000100402.69997.C3</identifier><identifier>PMID: 14551157</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cell Adhesion ; Cell Movement - drug effects ; Cells, Cultured ; Collagen - metabolism ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Extracellular Matrix - metabolism ; Gels ; Hyaluronan Receptors - physiology ; Hyperplasia ; Matrix Metalloproteinase 2 - deficiency ; Matrix Metalloproteinase 2 - genetics ; Matrix Metalloproteinase 2 - physiology ; Matrix Metalloproteinase 9 - deficiency ; Matrix Metalloproteinase 9 - genetics ; Matrix Metalloproteinase 9 - physiology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - enzymology ; Platelet-Derived Growth Factor - pharmacology ; Protease Inhibitors - pharmacology ; Proto-Oncogene Proteins c-sis ; Tunica Intima - pathology</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2004-01, Vol.24 (1), p.54-60</ispartof><rights>2004 American Heart Association, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jan 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5670-f5fc1c35850df01d754b1f71cd6475551e8e8f267eb56b1c3f78a124793938c93</citedby><cites>FETCH-LOGICAL-c5670-f5fc1c35850df01d754b1f71cd6475551e8e8f267eb56b1c3f78a124793938c93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,4026,27930,27931,27932</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15560513$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14551157$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Johnson, Chad</creatorcontrib><creatorcontrib>Galis, Zorina S</creatorcontrib><title>Matrix Metalloproteinase-2 and −9 Differentially Regulate Smooth Muscle Cell Migration and Cell-Mediated Collagen Organization</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVES—Smooth muscle cells (SMCs) produce both matrix metalloproteinase (MMP)-2 and MMP-9, enzymes with similar in vitro matrix degrading abilities. We compared the specific contributions of these enzymes to SMC-matrix interactions in vitro and in vivo.
METHODS AND RESULTS—Using genetic models of deficiency, we investigated MMP-2 and MMP-9 roles in SMC migration in vivo in the formation of intimal hyperplasia and in vitro. In addition, we investigated potential effects of MMP-2 and MMP-9 genetic deficiency on compaction and assembly of collagen by SMCs.
CONCLUSIONS—MMP-2 and MMP-9 genetic deficiency decreased by 81% and 65%, respectively (P <0.01), SMC invasion in vitro and decreased formation of intimal hyperplasia in vivo (P <0.01). However, we found that MMP-9, but not MMP-2, was necessary for organization of collagen by SMCs. Likewise, we found that MMP-9 deficiency resulted in a 50% reduction of SMC attachment to gelatin (P <0.01), indicating that SMCs may use MMP-9 as a bridge between the cell surface and matrix. Furthermore, we found that the hyaluronan receptor, CD44, assists in attachment and utilization of MMP-9 by SMCs. Understanding the specific roles of these MMPs, generally thought to be similar, could improve the design of therapeutic interventions aimed at controlling vascular remodeling.</description><subject>Animals</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cell Adhesion</subject><subject>Cell Movement - drug effects</subject><subject>Cells, Cultured</subject><subject>Collagen - metabolism</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Extracellular Matrix - metabolism</subject><subject>Gels</subject><subject>Hyaluronan Receptors - physiology</subject><subject>Hyperplasia</subject><subject>Matrix Metalloproteinase 2 - deficiency</subject><subject>Matrix Metalloproteinase 2 - genetics</subject><subject>Matrix Metalloproteinase 2 - physiology</subject><subject>Matrix Metalloproteinase 9 - deficiency</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Matrix Metalloproteinase 9 - physiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - enzymology</subject><subject>Platelet-Derived Growth Factor - pharmacology</subject><subject>Protease Inhibitors - pharmacology</subject><subject>Proto-Oncogene Proteins c-sis</subject><subject>Tunica Intima - pathology</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkctu1DAUhiMEoqXwCsiqBLsE352wq8JValQJClvL4xzPuHiSYicqZcWSNY_Ik-DMjDQS3vii7_znP_6L4pzgihBJXmFSXVx_rXBeBGOOaSWbplFVyx4Up0RQXnLJ5MN8xqopheT0pHiS0k3mOaX4cXFCuBCECHVa_OrMFP0P1MFkQhhv4ziBH0yCkiIz9Ojv7z8NeuOdgwjD5DNzjz7Beg5mAvR5O47TBnVzsgFQCyGgzq-jmfw47KqXp7KD3mc638YQzBoGdBXXZvA_d9zT4pEzIcGzw35WfHn39rr9UF5evf_YXlyWVkiFSyecJZaJWuDeYdIrwVfEKWJ7yZXI00ANtaNSwUrIVSadqg2hXDWsYbVt2Fnxcq-bR_w-Q5r01ieb_ZkBxjnpGuOayYZn8Pw_8Gac45C9aZr_r5ayXtRe7yEbx5QiOH0b_dbEe02wXkLSmOgckj6GpHch6Zbl4ueHDvNqC_2x9JBKBl4cAJOsCS6awfp05ISQWJBFiO-5uzFMENO3MN9B1BswYdosrTnLYEmX_tkELndm2D_QE6rk</recordid><startdate>200401</startdate><enddate>200401</enddate><creator>Johnson, Chad</creator><creator>Galis, Zorina S</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</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>K9.</scope><scope>7X8</scope></search><sort><creationdate>200401</creationdate><title>Matrix Metalloproteinase-2 and −9 Differentially Regulate Smooth Muscle Cell Migration and Cell-Mediated Collagen Organization</title><author>Johnson, Chad ; Galis, Zorina S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5670-f5fc1c35850df01d754b1f71cd6475551e8e8f267eb56b1c3f78a124793938c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cell Adhesion</topic><topic>Cell Movement - drug effects</topic><topic>Cells, Cultured</topic><topic>Collagen - metabolism</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Extracellular Matrix - metabolism</topic><topic>Gels</topic><topic>Hyaluronan Receptors - physiology</topic><topic>Hyperplasia</topic><topic>Matrix Metalloproteinase 2 - deficiency</topic><topic>Matrix Metalloproteinase 2 - genetics</topic><topic>Matrix Metalloproteinase 2 - physiology</topic><topic>Matrix Metalloproteinase 9 - deficiency</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Matrix Metalloproteinase 9 - physiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - enzymology</topic><topic>Platelet-Derived Growth Factor - pharmacology</topic><topic>Protease Inhibitors - pharmacology</topic><topic>Proto-Oncogene Proteins c-sis</topic><topic>Tunica Intima - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Johnson, Chad</creatorcontrib><creatorcontrib>Galis, Zorina S</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Johnson, Chad</au><au>Galis, Zorina S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Matrix Metalloproteinase-2 and −9 Differentially Regulate Smooth Muscle Cell Migration and Cell-Mediated Collagen Organization</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2004-01</date><risdate>2004</risdate><volume>24</volume><issue>1</issue><spage>54</spage><epage>60</epage><pages>54-60</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVES—Smooth muscle cells (SMCs) produce both matrix metalloproteinase (MMP)-2 and MMP-9, enzymes with similar in vitro matrix degrading abilities. We compared the specific contributions of these enzymes to SMC-matrix interactions in vitro and in vivo.
METHODS AND RESULTS—Using genetic models of deficiency, we investigated MMP-2 and MMP-9 roles in SMC migration in vivo in the formation of intimal hyperplasia and in vitro. In addition, we investigated potential effects of MMP-2 and MMP-9 genetic deficiency on compaction and assembly of collagen by SMCs.
CONCLUSIONS—MMP-2 and MMP-9 genetic deficiency decreased by 81% and 65%, respectively (P <0.01), SMC invasion in vitro and decreased formation of intimal hyperplasia in vivo (P <0.01). However, we found that MMP-9, but not MMP-2, was necessary for organization of collagen by SMCs. Likewise, we found that MMP-9 deficiency resulted in a 50% reduction of SMC attachment to gelatin (P <0.01), indicating that SMCs may use MMP-9 as a bridge between the cell surface and matrix. Furthermore, we found that the hyaluronan receptor, CD44, assists in attachment and utilization of MMP-9 by SMCs. Understanding the specific roles of these MMPs, generally thought to be similar, could improve the design of therapeutic interventions aimed at controlling vascular remodeling.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>14551157</pmid><doi>10.1161/01.ATV.0000100402.69997.C3</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2004-01, Vol.24 (1), p.54-60 |
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| subjects | Animals Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cell Adhesion Cell Movement - drug effects Cells, Cultured Collagen - metabolism Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Extracellular Matrix - metabolism Gels Hyaluronan Receptors - physiology Hyperplasia Matrix Metalloproteinase 2 - deficiency Matrix Metalloproteinase 2 - genetics Matrix Metalloproteinase 2 - physiology Matrix Metalloproteinase 9 - deficiency Matrix Metalloproteinase 9 - genetics Matrix Metalloproteinase 9 - physiology Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - enzymology Platelet-Derived Growth Factor - pharmacology Protease Inhibitors - pharmacology Proto-Oncogene Proteins c-sis Tunica Intima - pathology |
| title | Matrix Metalloproteinase-2 and −9 Differentially Regulate Smooth Muscle Cell Migration and Cell-Mediated Collagen Organization |
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