Matrix metalloproteinase-8 and -9 are increased at the site of abdominal aortic aneurysm rupture

Abdominal aortic aneurysm (AAA) expansion is characterized by extracellular matrix degradation and widespread inflammation. In contrast, the processes that characterize AAA rupture are not well understood. The aim of this study was to investigate the proteolytic and cellular activity of ruptured AAA...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 2006-01, Vol.113 (3), p.438-445
Hauptverfasser: WILSON, W. Richard W, ANDERTON, Marcus, SCHWALBE, Edward C, JONES, J. Louise, FURNESS, Peter N, BELL, Peter R. F, THOMPSON, Matthew M
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container_issue 3
container_start_page 438
container_title Circulation (New York, N.Y.)
container_volume 113
creator WILSON, W. Richard W
ANDERTON, Marcus
SCHWALBE, Edward C
JONES, J. Louise
FURNESS, Peter N
BELL, Peter R. F
THOMPSON, Matthew M
description Abdominal aortic aneurysm (AAA) expansion is characterized by extracellular matrix degradation and widespread inflammation. In contrast, the processes that characterize AAA rupture are not well understood. The aim of this study was to investigate the proteolytic and cellular activity of ruptured AAA, focusing on matrix metalloproteinases (MMPs) and their inhibitors (TIMPs). Anterior aneurysm wall biopsies were taken from 55 nonruptured and 21 ruptured AAAs. A further biopsy from the site of rupture was taken from 12 of the ruptured AAAs. MMP-1, -2, -3, -8, -9, and -13, as well as TIMP-1 and -2, were quantified in each biopsy with ELISA. A comparison of anterior aneurysm biopsies showed no difference in MMP or TIMP concentrations between nonruptured and ruptured AAA. In a comparison of ruptured AAA biopsies, MMP-8 and -9 levels were significantly elevated in the 12 rupture site biopsies compared with their 12 paired anterior wall biopsies, whereas other MMPs and TIMPs showed no difference (MMP-8, P
doi_str_mv 10.1161/CIRCULATIONAHA.105.551572
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Richard W ; ANDERTON, Marcus ; SCHWALBE, Edward C ; JONES, J. Louise ; FURNESS, Peter N ; BELL, Peter R. F ; THOMPSON, Matthew M</creator><creatorcontrib>WILSON, W. Richard W ; ANDERTON, Marcus ; SCHWALBE, Edward C ; JONES, J. Louise ; FURNESS, Peter N ; BELL, Peter R. F ; THOMPSON, Matthew M</creatorcontrib><description>Abdominal aortic aneurysm (AAA) expansion is characterized by extracellular matrix degradation and widespread inflammation. In contrast, the processes that characterize AAA rupture are not well understood. The aim of this study was to investigate the proteolytic and cellular activity of ruptured AAA, focusing on matrix metalloproteinases (MMPs) and their inhibitors (TIMPs). Anterior aneurysm wall biopsies were taken from 55 nonruptured and 21 ruptured AAAs. A further biopsy from the site of rupture was taken from 12 of the ruptured AAAs. MMP-1, -2, -3, -8, -9, and -13, as well as TIMP-1 and -2, were quantified in each biopsy with ELISA. A comparison of anterior aneurysm biopsies showed no difference in MMP or TIMP concentrations between nonruptured and ruptured AAA. In a comparison of ruptured AAA biopsies, MMP-8 and -9 levels were significantly elevated in the 12 rupture site biopsies compared with their 12 paired anterior wall biopsies, whereas other MMPs and TIMPs showed no difference (MMP-8, P&lt;0.001; MMP-9, P=0.01). MMP-8 and -9 expression was mediated by native mesenchymal cells and was independent of the inflammatory infiltrate. A localized increase in MMP-8 and -9, mediated by native mesenchymal cells, presents a potential pathway for collagen breakdown and AAA rupture.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/CIRCULATIONAHA.105.551572</identifier><identifier>PMID: 16432074</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams &amp; Wilkins</publisher><subject>Aged ; Aorta, Abdominal - enzymology ; Aorta, Abdominal - pathology ; Aortic Aneurysm, Abdominal - metabolism ; Aortic Aneurysm, Abdominal - pathology ; Aortic Rupture - metabolism ; Aortic Rupture - pathology ; Biological and medical sciences ; Biopsy ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cardiovascular system ; Collagen - metabolism ; Diseases of the aorta ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Female ; Gene Expression Regulation, Enzymologic ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; Male ; Matrix Metalloproteinase 8 - genetics ; Matrix Metalloproteinase 8 - metabolism ; Matrix Metalloproteinase 9 - genetics ; Matrix Metalloproteinase 9 - metabolism ; Medical sciences ; Mesoderm - enzymology ; Mesoderm - pathology ; Radiodiagnosis. Nmr imagery. 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Richard W</creatorcontrib><creatorcontrib>ANDERTON, Marcus</creatorcontrib><creatorcontrib>SCHWALBE, Edward C</creatorcontrib><creatorcontrib>JONES, J. Louise</creatorcontrib><creatorcontrib>FURNESS, Peter N</creatorcontrib><creatorcontrib>BELL, Peter R. F</creatorcontrib><creatorcontrib>THOMPSON, Matthew M</creatorcontrib><title>Matrix metalloproteinase-8 and -9 are increased at the site of abdominal aortic aneurysm rupture</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Abdominal aortic aneurysm (AAA) expansion is characterized by extracellular matrix degradation and widespread inflammation. In contrast, the processes that characterize AAA rupture are not well understood. The aim of this study was to investigate the proteolytic and cellular activity of ruptured AAA, focusing on matrix metalloproteinases (MMPs) and their inhibitors (TIMPs). Anterior aneurysm wall biopsies were taken from 55 nonruptured and 21 ruptured AAAs. A further biopsy from the site of rupture was taken from 12 of the ruptured AAAs. MMP-1, -2, -3, -8, -9, and -13, as well as TIMP-1 and -2, were quantified in each biopsy with ELISA. A comparison of anterior aneurysm biopsies showed no difference in MMP or TIMP concentrations between nonruptured and ruptured AAA. In a comparison of ruptured AAA biopsies, MMP-8 and -9 levels were significantly elevated in the 12 rupture site biopsies compared with their 12 paired anterior wall biopsies, whereas other MMPs and TIMPs showed no difference (MMP-8, P&lt;0.001; MMP-9, P=0.01). MMP-8 and -9 expression was mediated by native mesenchymal cells and was independent of the inflammatory infiltrate. A localized increase in MMP-8 and -9, mediated by native mesenchymal cells, presents a potential pathway for collagen breakdown and AAA rupture.</description><subject>Aged</subject><subject>Aorta, Abdominal - enzymology</subject><subject>Aorta, Abdominal - pathology</subject><subject>Aortic Aneurysm, Abdominal - metabolism</subject><subject>Aortic Aneurysm, Abdominal - pathology</subject><subject>Aortic Rupture - metabolism</subject><subject>Aortic Rupture - pathology</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular system</subject><subject>Collagen - metabolism</subject><subject>Diseases of the aorta</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Female</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Humans</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Male</subject><subject>Matrix Metalloproteinase 8 - genetics</subject><subject>Matrix Metalloproteinase 8 - metabolism</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medical sciences</subject><subject>Mesoderm - enzymology</subject><subject>Mesoderm - pathology</subject><subject>Radiodiagnosis. Nmr imagery. 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F ; THOMPSON, Matthew M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-422265c754af611745f4034842264b93047e2350197751e0b0517e44eb1353513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Aged</topic><topic>Aorta, Abdominal - enzymology</topic><topic>Aorta, Abdominal - pathology</topic><topic>Aortic Aneurysm, Abdominal - metabolism</topic><topic>Aortic Aneurysm, Abdominal - pathology</topic><topic>Aortic Rupture - metabolism</topic><topic>Aortic Rupture - pathology</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular system</topic><topic>Collagen - metabolism</topic><topic>Diseases of the aorta</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Female</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Humans</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Male</topic><topic>Matrix Metalloproteinase 8 - genetics</topic><topic>Matrix Metalloproteinase 8 - metabolism</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medical sciences</topic><topic>Mesoderm - enzymology</topic><topic>Mesoderm - pathology</topic><topic>Radiodiagnosis. Nmr imagery. Nmr spectrometry</topic><topic>Vasculitis - metabolism</topic><topic>Vasculitis - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WILSON, W. Richard W</creatorcontrib><creatorcontrib>ANDERTON, Marcus</creatorcontrib><creatorcontrib>SCHWALBE, Edward C</creatorcontrib><creatorcontrib>JONES, J. Louise</creatorcontrib><creatorcontrib>FURNESS, Peter N</creatorcontrib><creatorcontrib>BELL, Peter R. F</creatorcontrib><creatorcontrib>THOMPSON, Matthew M</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>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WILSON, W. Richard W</au><au>ANDERTON, Marcus</au><au>SCHWALBE, Edward C</au><au>JONES, J. Louise</au><au>FURNESS, Peter N</au><au>BELL, Peter R. F</au><au>THOMPSON, Matthew M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Matrix metalloproteinase-8 and -9 are increased at the site of abdominal aortic aneurysm rupture</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2006-01-24</date><risdate>2006</risdate><volume>113</volume><issue>3</issue><spage>438</spage><epage>445</epage><pages>438-445</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Abdominal aortic aneurysm (AAA) expansion is characterized by extracellular matrix degradation and widespread inflammation. In contrast, the processes that characterize AAA rupture are not well understood. The aim of this study was to investigate the proteolytic and cellular activity of ruptured AAA, focusing on matrix metalloproteinases (MMPs) and their inhibitors (TIMPs). Anterior aneurysm wall biopsies were taken from 55 nonruptured and 21 ruptured AAAs. A further biopsy from the site of rupture was taken from 12 of the ruptured AAAs. MMP-1, -2, -3, -8, -9, and -13, as well as TIMP-1 and -2, were quantified in each biopsy with ELISA. A comparison of anterior aneurysm biopsies showed no difference in MMP or TIMP concentrations between nonruptured and ruptured AAA. In a comparison of ruptured AAA biopsies, MMP-8 and -9 levels were significantly elevated in the 12 rupture site biopsies compared with their 12 paired anterior wall biopsies, whereas other MMPs and TIMPs showed no difference (MMP-8, P&lt;0.001; MMP-9, P=0.01). MMP-8 and -9 expression was mediated by native mesenchymal cells and was independent of the inflammatory infiltrate. A localized increase in MMP-8 and -9, mediated by native mesenchymal cells, presents a potential pathway for collagen breakdown and AAA rupture.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams &amp; Wilkins</pub><pmid>16432074</pmid><doi>10.1161/CIRCULATIONAHA.105.551572</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals
subjects Aged
Aorta, Abdominal - enzymology
Aorta, Abdominal - pathology
Aortic Aneurysm, Abdominal - metabolism
Aortic Aneurysm, Abdominal - pathology
Aortic Rupture - metabolism
Aortic Rupture - pathology
Biological and medical sciences
Biopsy
Blood and lymphatic vessels
Cardiology. Vascular system
Cardiovascular system
Collagen - metabolism
Diseases of the aorta
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Female
Gene Expression Regulation, Enzymologic
Humans
Investigative techniques, diagnostic techniques (general aspects)
Male
Matrix Metalloproteinase 8 - genetics
Matrix Metalloproteinase 8 - metabolism
Matrix Metalloproteinase 9 - genetics
Matrix Metalloproteinase 9 - metabolism
Medical sciences
Mesoderm - enzymology
Mesoderm - pathology
Radiodiagnosis. Nmr imagery. Nmr spectrometry
Vasculitis - metabolism
Vasculitis - pathology
title Matrix metalloproteinase-8 and -9 are increased at the site of abdominal aortic aneurysm rupture
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