Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques
We hypothesized that collagenolytic activity produced by activated macrophages contributes to collagen loss and the subsequent instability of atheromatous lesions, a common trigger of acute coronary syndromes. However, no direct in vivo evidence links collagenases with the regulation of collagen con...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2004-10, Vol.110 (14), p.1953-1959 |
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| container_title | Circulation (New York, N.Y.) |
| container_volume | 110 |
| creator | FUKUMOTO, Yoshihiro DEGUCHI, Jun-O KRANE, Stephen M AIKAWA, Masanori LIBBY, Peter RABKIN-AIKAWA, Elena SAKATA, Yasuhiko CHIN, Michael T HILL, Christopher C LAWLER, Patrick R VARO, Nerea SCHOEN, Frederick J |
| description | We hypothesized that collagenolytic activity produced by activated macrophages contributes to collagen loss and the subsequent instability of atheromatous lesions, a common trigger of acute coronary syndromes. However, no direct in vivo evidence links collagenases with the regulation of collagen content in atherosclerotic plaques.
To test the hypothesis that collagenases influence the structure of atheromata, we examined collagen accumulation in atherosclerotic lesions of apolipoprotein E-deficient mice (apoE-/-) that express collagenase-resistant collagen-I (ColR/R/apoE-/-, n=12) or wild-type collagen-expressing mice (Col+/+/apoE-/-, n=12). Aortic atheromata of both groups had similar sizes and numbers of macrophages, a major source of collagenases. However, aortic intimas from ColR/R/apoE-/- mice contained fewer smooth muscle cells, a source of collagen, probably because of decreased migration or proliferation or increased cell death. Despite reduced numbers of smooth muscle cells, atheromata of ColR/R/apoE-/- mice contained significantly more intimal collagen than did those of Col+/+/apoE-/- mice.
These results establish that collagenase action regulates plaque collagen turnover and smooth muscle cell accumulation. |
| doi_str_mv | 10.1161/01.CIR.0000143174.41810.10 |
| format | Article |
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To test the hypothesis that collagenases influence the structure of atheromata, we examined collagen accumulation in atherosclerotic lesions of apolipoprotein E-deficient mice (apoE-/-) that express collagenase-resistant collagen-I (ColR/R/apoE-/-, n=12) or wild-type collagen-expressing mice (Col+/+/apoE-/-, n=12). Aortic atheromata of both groups had similar sizes and numbers of macrophages, a major source of collagenases. However, aortic intimas from ColR/R/apoE-/- mice contained fewer smooth muscle cells, a source of collagen, probably because of decreased migration or proliferation or increased cell death. Despite reduced numbers of smooth muscle cells, atheromata of ColR/R/apoE-/- mice contained significantly more intimal collagen than did those of Col+/+/apoE-/- mice.
These results establish that collagenase action regulates plaque collagen turnover and smooth muscle cell accumulation.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000143174.41810.10</identifier><identifier>PMID: 15451791</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Amino Acid Substitution ; Animals ; Apolipoproteins E - deficiency ; Apolipoproteins E - genetics ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cardiovascular system ; Cell Count ; Cell Death ; Cell Movement ; Collagen Type I - genetics ; Collagen Type I - metabolism ; Collagenases - metabolism ; Coronary Artery Disease - enzymology ; Coronary Artery Disease - genetics ; Coronary Artery Disease - pathology ; Crosses, Genetic ; Diet, Atherogenic ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Macrophages - enzymology ; Macrophages, Peritoneal - enzymology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Miscellaneous ; Muscle, Smooth, Vascular - pathology ; Pharmacology. Drug treatments ; Substrate Specificity - genetics ; Tunica Intima - pathology</subject><ispartof>Circulation (New York, N.Y.), 2004-10, Vol.110 (14), p.1953-1959</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-6f5a1839f9574de61a5f0ea0a272cfb48fb90f83d4c70f844f4cd1903ebe7c263</citedby><cites>FETCH-LOGICAL-c539t-6f5a1839f9574de61a5f0ea0a272cfb48fb90f83d4c70f844f4cd1903ebe7c263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16550104$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15451791$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FUKUMOTO, Yoshihiro</creatorcontrib><creatorcontrib>DEGUCHI, Jun-O</creatorcontrib><creatorcontrib>KRANE, Stephen M</creatorcontrib><creatorcontrib>AIKAWA, Masanori</creatorcontrib><creatorcontrib>LIBBY, Peter</creatorcontrib><creatorcontrib>RABKIN-AIKAWA, Elena</creatorcontrib><creatorcontrib>SAKATA, Yasuhiko</creatorcontrib><creatorcontrib>CHIN, Michael T</creatorcontrib><creatorcontrib>HILL, Christopher C</creatorcontrib><creatorcontrib>LAWLER, Patrick R</creatorcontrib><creatorcontrib>VARO, Nerea</creatorcontrib><creatorcontrib>SCHOEN, Frederick J</creatorcontrib><title>Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>We hypothesized that collagenolytic activity produced by activated macrophages contributes to collagen loss and the subsequent instability of atheromatous lesions, a common trigger of acute coronary syndromes. However, no direct in vivo evidence links collagenases with the regulation of collagen content in atherosclerotic plaques.
To test the hypothesis that collagenases influence the structure of atheromata, we examined collagen accumulation in atherosclerotic lesions of apolipoprotein E-deficient mice (apoE-/-) that express collagenase-resistant collagen-I (ColR/R/apoE-/-, n=12) or wild-type collagen-expressing mice (Col+/+/apoE-/-, n=12). Aortic atheromata of both groups had similar sizes and numbers of macrophages, a major source of collagenases. However, aortic intimas from ColR/R/apoE-/- mice contained fewer smooth muscle cells, a source of collagen, probably because of decreased migration or proliferation or increased cell death. Despite reduced numbers of smooth muscle cells, atheromata of ColR/R/apoE-/- mice contained significantly more intimal collagen than did those of Col+/+/apoE-/- mice.
These results establish that collagenase action regulates plaque collagen turnover and smooth muscle cell accumulation.</description><subject>Amino Acid Substitution</subject><subject>Animals</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - genetics</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>Cardiovascular system</subject><subject>Cell Count</subject><subject>Cell Death</subject><subject>Cell Movement</subject><subject>Collagen Type I - genetics</subject><subject>Collagen Type I - metabolism</subject><subject>Collagenases - metabolism</subject><subject>Coronary Artery Disease - enzymology</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary Artery Disease - pathology</subject><subject>Crosses, Genetic</subject><subject>Diet, Atherogenic</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Macrophages - enzymology</subject><subject>Macrophages, Peritoneal - enzymology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Miscellaneous</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Substrate Specificity - genetics</subject><subject>Tunica Intima - pathology</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctKLDEQQINc0fHxC9II112PqU7SD3cy-AJBEF2HTLqiuaS753bSCzd-uzXj4CzNIqGoU6lUDmPnwOcAJVxymC8enuecFkgBlZxLqNdJvsdmoAqZSyWaP2xGQJNXoigO2VGM_ygsRaUO2CEoqaBqYMY-77DH5K0J4SNrMeHY-R7bbMToYzK9xSwNmR1CMG_Ym4iZsckPfWamtw77FDPfU1FMPnkTfkCi7NRNwWxYT3F6x3GINtBO7bJVMP8njCds35kQ8XR7HrPX25uXxX3--HT3sLh-zC1NkvLSKQO1aFyjKtliCUY5joaboiqsW8raLRvuatFKW9EppZO2hYYLXGJli1Ics4vve1fjsO6bdOejRXpsj8MUdVk2gj4NfgULKASv5Rq8-gYtjRVHdHo1-s6MHxq4XmvSHDRp0jtNeqOJ8lR8tu0yLTtsd6VbLwT83QImkhs3kgkfd1ypFAcuxRc1_Z8N</recordid><startdate>20041005</startdate><enddate>20041005</enddate><creator>FUKUMOTO, Yoshihiro</creator><creator>DEGUCHI, Jun-O</creator><creator>KRANE, Stephen M</creator><creator>AIKAWA, Masanori</creator><creator>LIBBY, Peter</creator><creator>RABKIN-AIKAWA, Elena</creator><creator>SAKATA, Yasuhiko</creator><creator>CHIN, Michael T</creator><creator>HILL, Christopher C</creator><creator>LAWLER, Patrick R</creator><creator>VARO, Nerea</creator><creator>SCHOEN, Frederick J</creator><general>Lippincott Williams & Wilkins</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20041005</creationdate><title>Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques</title><author>FUKUMOTO, Yoshihiro ; DEGUCHI, Jun-O ; KRANE, Stephen M ; AIKAWA, Masanori ; LIBBY, Peter ; RABKIN-AIKAWA, Elena ; SAKATA, Yasuhiko ; CHIN, Michael T ; HILL, Christopher C ; LAWLER, Patrick R ; VARO, Nerea ; SCHOEN, Frederick J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c539t-6f5a1839f9574de61a5f0ea0a272cfb48fb90f83d4c70f844f4cd1903ebe7c263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Amino Acid Substitution</topic><topic>Animals</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - genetics</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>Cardiovascular system</topic><topic>Cell Count</topic><topic>Cell Death</topic><topic>Cell Movement</topic><topic>Collagen Type I - genetics</topic><topic>Collagen Type I - metabolism</topic><topic>Collagenases - metabolism</topic><topic>Coronary Artery Disease - enzymology</topic><topic>Coronary Artery Disease - genetics</topic><topic>Coronary Artery Disease - pathology</topic><topic>Crosses, Genetic</topic><topic>Diet, Atherogenic</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Macrophages - enzymology</topic><topic>Macrophages, Peritoneal - enzymology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Miscellaneous</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Substrate Specificity - genetics</topic><topic>Tunica Intima - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FUKUMOTO, Yoshihiro</creatorcontrib><creatorcontrib>DEGUCHI, Jun-O</creatorcontrib><creatorcontrib>KRANE, Stephen M</creatorcontrib><creatorcontrib>AIKAWA, Masanori</creatorcontrib><creatorcontrib>LIBBY, Peter</creatorcontrib><creatorcontrib>RABKIN-AIKAWA, Elena</creatorcontrib><creatorcontrib>SAKATA, Yasuhiko</creatorcontrib><creatorcontrib>CHIN, Michael T</creatorcontrib><creatorcontrib>HILL, Christopher C</creatorcontrib><creatorcontrib>LAWLER, Patrick R</creatorcontrib><creatorcontrib>VARO, Nerea</creatorcontrib><creatorcontrib>SCHOEN, Frederick J</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</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>FUKUMOTO, Yoshihiro</au><au>DEGUCHI, Jun-O</au><au>KRANE, Stephen M</au><au>AIKAWA, Masanori</au><au>LIBBY, Peter</au><au>RABKIN-AIKAWA, Elena</au><au>SAKATA, Yasuhiko</au><au>CHIN, Michael T</au><au>HILL, Christopher C</au><au>LAWLER, Patrick R</au><au>VARO, Nerea</au><au>SCHOEN, Frederick J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2004-10-05</date><risdate>2004</risdate><volume>110</volume><issue>14</issue><spage>1953</spage><epage>1959</epage><pages>1953-1959</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>We hypothesized that collagenolytic activity produced by activated macrophages contributes to collagen loss and the subsequent instability of atheromatous lesions, a common trigger of acute coronary syndromes. However, no direct in vivo evidence links collagenases with the regulation of collagen content in atherosclerotic plaques.
To test the hypothesis that collagenases influence the structure of atheromata, we examined collagen accumulation in atherosclerotic lesions of apolipoprotein E-deficient mice (apoE-/-) that express collagenase-resistant collagen-I (ColR/R/apoE-/-, n=12) or wild-type collagen-expressing mice (Col+/+/apoE-/-, n=12). Aortic atheromata of both groups had similar sizes and numbers of macrophages, a major source of collagenases. However, aortic intimas from ColR/R/apoE-/- mice contained fewer smooth muscle cells, a source of collagen, probably because of decreased migration or proliferation or increased cell death. Despite reduced numbers of smooth muscle cells, atheromata of ColR/R/apoE-/- mice contained significantly more intimal collagen than did those of Col+/+/apoE-/- mice.
These results establish that collagenase action regulates plaque collagen turnover and smooth muscle cell accumulation.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>15451791</pmid><doi>10.1161/01.CIR.0000143174.41810.10</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2004-10, Vol.110 (14), p.1953-1959 |
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| source | MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals; Journals@Ovid Complete |
| subjects | Amino Acid Substitution Animals Apolipoproteins E - deficiency Apolipoproteins E - genetics Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiovascular system Cell Count Cell Death Cell Movement Collagen Type I - genetics Collagen Type I - metabolism Collagenases - metabolism Coronary Artery Disease - enzymology Coronary Artery Disease - genetics Coronary Artery Disease - pathology Crosses, Genetic Diet, Atherogenic Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Macrophages - enzymology Macrophages, Peritoneal - enzymology Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Miscellaneous Muscle, Smooth, Vascular - pathology Pharmacology. Drug treatments Substrate Specificity - genetics Tunica Intima - pathology |
| title | Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques |
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