Compensatory Vascular Remodeling During Atherosclerotic Lesion Growth Depends on Matrix Metalloproteinase-9 Activity
OBJECTIVE—The compensatory arterial remodeling associated with atherosclerotic plaques is thought to rely on the activity of matrix metalloproteinases (MMP). To assess the role of MMP-9, we analyzed the effect of MMP-9 genetic deficiency on the development and remodeling of experimental atherosclero...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2004-11, Vol.24 (11), p.2123-2129 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Lessner, Susan M Martinson, Deborah E Galis, Zorina S |
| description | OBJECTIVE—The compensatory arterial remodeling associated with atherosclerotic plaques is thought to rely on the activity of matrix metalloproteinases (MMP). To assess the role of MMP-9, we analyzed the effect of MMP-9 genetic deficiency on the development and remodeling of experimental atherosclerotic lesions induced in the apolipoprotein E (apoE) knockout (−/−) mouse model.
METHODS AND RESULTS—We analyzed remodeling parameters and cellular composition of experimental carotid artery atherosclerotic lesions in apoE−/− and apoE−/− MMP-9−/− double-knockout (DKO) mice at 0, 3, 7, and 14 days after induction by flow cessation. Morphometric image analysis of arterial tissue sections indicated that overall artery size, measured as area encompassed by the external elastic lamina, increased 3.1-fold in the apoE−/− mice but only 1.6-fold in the DKO mice (P |
| doi_str_mv | 10.1161/01.ATV.0000141840.27300.fd |
| format | Article |
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METHODS AND RESULTS—We analyzed remodeling parameters and cellular composition of experimental carotid artery atherosclerotic lesions in apoE−/− and apoE−/− MMP-9−/− double-knockout (DKO) mice at 0, 3, 7, and 14 days after induction by flow cessation. Morphometric image analysis of arterial tissue sections indicated that overall artery size, measured as area encompassed by the external elastic lamina, increased 3.1-fold in the apoE−/− mice but only 1.6-fold in the DKO mice (P<0.0001) by 14 days. At the same time, the net lesion area occupied by macrophages was similar. Statistical analysis indicated that the overall expansion of the artery was 2.5-fold less sensitive to macrophage content in DKO compared with apoE−/− mice. No compensatory increase in other gelatinolytic activities was detected in the DKO.
CONCLUSIONS—MMP-9 deficiency significantly impaired compensatory vessel enlargement during carotid artery lesion development in the apoE−/− mouse, without altering macrophage content of lesions.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000141840.27300.fd</identifier><identifier>PMID: 15308548</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Apolipoproteins E - deficiency ; Apolipoproteins E - physiology ; Arteriosclerosis - enzymology ; Arteriosclerosis - pathology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Vessels - enzymology ; Blood Vessels - metabolism ; Blood Vessels - pathology ; Blood vessels and receptors ; Breeding ; Cardiology. Vascular system ; Carotid Arteries - pathology ; Collagen - metabolism ; Disease Models, Animal ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Fundamental and applied biological sciences. Psychology ; Macrophages - metabolism ; Matrix Metalloproteinase 2 - biosynthesis ; Matrix Metalloproteinase 2 - physiology ; Matrix Metalloproteinase 9 - deficiency ; Matrix Metalloproteinase 9 - physiology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Vertebrates: cardiovascular system</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2004-11, Vol.24 (11), p.2123-2129</ispartof><rights>2004 American Heart Association, Inc.</rights><rights>2005 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5705-e307f759b76135ce9db1ec1cd33e9998261075652d38bfdd6f008326241270823</citedby><cites>FETCH-LOGICAL-c5705-e307f759b76135ce9db1ec1cd33e9998261075652d38bfdd6f008326241270823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16277100$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15308548$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lessner, Susan M</creatorcontrib><creatorcontrib>Martinson, Deborah E</creatorcontrib><creatorcontrib>Galis, Zorina S</creatorcontrib><title>Compensatory Vascular Remodeling During Atherosclerotic Lesion Growth Depends on Matrix Metalloproteinase-9 Activity</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—The compensatory arterial remodeling associated with atherosclerotic plaques is thought to rely on the activity of matrix metalloproteinases (MMP). To assess the role of MMP-9, we analyzed the effect of MMP-9 genetic deficiency on the development and remodeling of experimental atherosclerotic lesions induced in the apolipoprotein E (apoE) knockout (−/−) mouse model.
METHODS AND RESULTS—We analyzed remodeling parameters and cellular composition of experimental carotid artery atherosclerotic lesions in apoE−/− and apoE−/− MMP-9−/− double-knockout (DKO) mice at 0, 3, 7, and 14 days after induction by flow cessation. Morphometric image analysis of arterial tissue sections indicated that overall artery size, measured as area encompassed by the external elastic lamina, increased 3.1-fold in the apoE−/− mice but only 1.6-fold in the DKO mice (P<0.0001) by 14 days. At the same time, the net lesion area occupied by macrophages was similar. Statistical analysis indicated that the overall expansion of the artery was 2.5-fold less sensitive to macrophage content in DKO compared with apoE−/− mice. No compensatory increase in other gelatinolytic activities was detected in the DKO.
CONCLUSIONS—MMP-9 deficiency significantly impaired compensatory vessel enlargement during carotid artery lesion development in the apoE−/− mouse, without altering macrophage content of lesions.</description><subject>Animals</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - physiology</subject><subject>Arteriosclerosis - enzymology</subject><subject>Arteriosclerosis - pathology</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Vessels - enzymology</subject><subject>Blood Vessels - metabolism</subject><subject>Blood Vessels - pathology</subject><subject>Blood vessels and receptors</subject><subject>Breeding</subject><subject>Cardiology. Vascular system</subject><subject>Carotid Arteries - pathology</subject><subject>Collagen - metabolism</subject><subject>Disease Models, Animal</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Macrophages - metabolism</subject><subject>Matrix Metalloproteinase 2 - biosynthesis</subject><subject>Matrix Metalloproteinase 2 - physiology</subject><subject>Matrix Metalloproteinase 9 - deficiency</subject><subject>Matrix Metalloproteinase 9 - physiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred Strains</subject><subject>Vertebrates: cardiovascular system</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>eNpdkW2LEzEQxxdRvPP0K8hyoO-2Tp53fVd6ego9BDnvbUizs3bPdLcmWWu_vdNroWBgMkP4zUPmXxTXDGaMafYB2Gx-_zADOkyyWsKMGwEw69pnxSVTXFZSC_2cYjBNpbTkF8WrlB6Jl5zDy-KCKQG1kvVlkRfjZotDcnmM-_LBJT8FF8vvuBlbDP3ws7yZ4sHN8xrjmHygO_e-XGLqx6G8jeMur8sbpCJtKunlzuXY_y3vMLsQxi3R2A8uYdWUc5_7P33evy5edC4kfHPyV8WPz5_uF1-q5bfbr4v5svLKgKpQgOmMalZGM6E8Nu2KoWe-FQKbpqm5pg8qrXgr6lXXtroDqAXXXDJuoObiqnh_rEtT_J4wZbvpk8cQ3IDjlKw2IIUCIPD6P_BxnOJAs1lOCIe6MQR9PEKe9pAidnYb-42Le8vAHoSxwCwJY8_C2CdhbNdS8ttTh2m1wfacelKCgHcngDRwoYtu8H06c5obw55GlUduN4aMMf0K0w6jXaMLeX1oLYWm3XEKGPFQkXEl_gEWPKa5</recordid><startdate>200411</startdate><enddate>200411</enddate><creator>Lessner, Susan M</creator><creator>Martinson, Deborah E</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>200411</creationdate><title>Compensatory Vascular Remodeling During Atherosclerotic Lesion Growth Depends on Matrix Metalloproteinase-9 Activity</title><author>Lessner, Susan M ; Martinson, Deborah E ; Galis, Zorina S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5705-e307f759b76135ce9db1ec1cd33e9998261075652d38bfdd6f008326241270823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - physiology</topic><topic>Arteriosclerosis - enzymology</topic><topic>Arteriosclerosis - pathology</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Vessels - enzymology</topic><topic>Blood Vessels - metabolism</topic><topic>Blood Vessels - pathology</topic><topic>Blood vessels and receptors</topic><topic>Breeding</topic><topic>Cardiology. Vascular system</topic><topic>Carotid Arteries - pathology</topic><topic>Collagen - metabolism</topic><topic>Disease Models, Animal</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Macrophages - metabolism</topic><topic>Matrix Metalloproteinase 2 - biosynthesis</topic><topic>Matrix Metalloproteinase 2 - physiology</topic><topic>Matrix Metalloproteinase 9 - deficiency</topic><topic>Matrix Metalloproteinase 9 - physiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred Strains</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lessner, Susan M</creatorcontrib><creatorcontrib>Martinson, Deborah E</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>Lessner, Susan M</au><au>Martinson, Deborah E</au><au>Galis, Zorina S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Compensatory Vascular Remodeling During Atherosclerotic Lesion Growth Depends on Matrix Metalloproteinase-9 Activity</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2004-11</date><risdate>2004</risdate><volume>24</volume><issue>11</issue><spage>2123</spage><epage>2129</epage><pages>2123-2129</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVE—The compensatory arterial remodeling associated with atherosclerotic plaques is thought to rely on the activity of matrix metalloproteinases (MMP). To assess the role of MMP-9, we analyzed the effect of MMP-9 genetic deficiency on the development and remodeling of experimental atherosclerotic lesions induced in the apolipoprotein E (apoE) knockout (−/−) mouse model.
METHODS AND RESULTS—We analyzed remodeling parameters and cellular composition of experimental carotid artery atherosclerotic lesions in apoE−/− and apoE−/− MMP-9−/− double-knockout (DKO) mice at 0, 3, 7, and 14 days after induction by flow cessation. Morphometric image analysis of arterial tissue sections indicated that overall artery size, measured as area encompassed by the external elastic lamina, increased 3.1-fold in the apoE−/− mice but only 1.6-fold in the DKO mice (P<0.0001) by 14 days. At the same time, the net lesion area occupied by macrophages was similar. Statistical analysis indicated that the overall expansion of the artery was 2.5-fold less sensitive to macrophage content in DKO compared with apoE−/− mice. No compensatory increase in other gelatinolytic activities was detected in the DKO.
CONCLUSIONS—MMP-9 deficiency significantly impaired compensatory vessel enlargement during carotid artery lesion development in the apoE−/− mouse, without altering macrophage content of lesions.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>15308548</pmid><doi>10.1161/01.ATV.0000141840.27300.fd</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2004-11, Vol.24 (11), p.2123-2129 |
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| subjects | Animals Apolipoproteins E - deficiency Apolipoproteins E - physiology Arteriosclerosis - enzymology Arteriosclerosis - pathology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Blood Vessels - enzymology Blood Vessels - metabolism Blood Vessels - pathology Blood vessels and receptors Breeding Cardiology. Vascular system Carotid Arteries - pathology Collagen - metabolism Disease Models, Animal Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Fundamental and applied biological sciences. Psychology Macrophages - metabolism Matrix Metalloproteinase 2 - biosynthesis Matrix Metalloproteinase 2 - physiology Matrix Metalloproteinase 9 - deficiency Matrix Metalloproteinase 9 - physiology Medical sciences Mice Mice, Inbred C57BL Mice, Inbred Strains Vertebrates: cardiovascular system |
| title | Compensatory Vascular Remodeling During Atherosclerotic Lesion Growth Depends on Matrix Metalloproteinase-9 Activity |
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