Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata
Aims Collagen degradation in atherosclerotic plaques with thin fibrous caps renders them more prone to rupture. Fibroblast activation protein (FAP) plays a role in arthritis and tumour formation through its collagenase activity. However, the significance of FAP in thin-cap human fibroatheromata rema...
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| creator | Brokopp, Chad E. Schoenauer, Roman Richards, Peter Bauer, Stefan Lohmann, Christine Emmert, Maximilian Y. Weber, Benedikt Winnik, Stephan Aikawa, Elena Graves, Kirk Genoni, Michele Vogt, Peter Lüscher, Thomas F. Renner, Christoph Hoerstrup, Simon P. Matter, Christian M. |
| description | Aims
Collagen degradation in atherosclerotic plaques with thin fibrous caps renders them more prone to rupture. Fibroblast activation protein (FAP) plays a role in arthritis and tumour formation through its collagenase activity. However, the significance of FAP in thin-cap human fibroatheromata remains unknown.
Methods and results
We detected enhanced FAP expression in type IV-V human aortic atheromata (n = 12), compared with type II-III lesions (n = 9; P < 0.01) and healthy aortae (n = 8; P < 0.01) by immunostaining and western blot analyses. Fibroblast activation protein was also increased in thin-cap ( |
| doi_str_mv | 10.1093/eurheartj/ehq519 |
| format | Article |
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Collagen degradation in atherosclerotic plaques with thin fibrous caps renders them more prone to rupture. Fibroblast activation protein (FAP) plays a role in arthritis and tumour formation through its collagenase activity. However, the significance of FAP in thin-cap human fibroatheromata remains unknown.
Methods and results
We detected enhanced FAP expression in type IV-V human aortic atheromata (n = 12), compared with type II-III lesions (n = 9; P < 0.01) and healthy aortae (n = 8; P < 0.01) by immunostaining and western blot analyses. Fibroblast activation protein was also increased in thin-cap (<65 µm) vs. thick-cap (≥65 µm) human coronary fibroatheromata (n = 12; P < 0.01). Fibroblast activation protein was expressed by human aortic smooth muscle cells (HASMC) as shown by colocalization on immunofluorescent aortic plaque stainings (n = 10; P < 0.01) and by flow cytometry in cell culture. Although macrophages did not express FAP, macrophage burden in human aortic plaques correlated with FAP expression (n = 12; R
2= 0.763; P < 0.05). Enzyme-linked immunosorbent assays showed a time- and dose-dependent up-regulation of FAP in response to human tumour necrosis factor α (TNFα) in HASMC (n = 6; P < 0.01). Moreover, supernatants from peripheral blood-derived macrophages induced FAP expression in cultured HASMC (n = 6; P < 0.01), an effect abolished by blocking TNFα (n = 6; P < 0.01). Fibroblast activation protein associated with collagen-poor regions in human coronary fibrous caps and digested type I collagen and gelatin in vitro (n = 6; P < 0.01). Zymography revealed that FAP-mediated collagenase activity was neutralized by an antibody directed against the FAP catalytic domain both in HASMC (n = 6; P < 0.01) and in fibrous caps of atherosclerotic plaques (n = 10; P < 0.01).
Conclusion
Fibroblast activation protein expression in HASMC is induced by macrophage-derived TNFα. Fibroblast activation protein associates with thin-cap human coronary fibroatheromata and contributes to type I collagen breakdown in fibrous caps.]]></description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehq519</identifier><identifier>PMID: 21292680</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Aged ; Analysis of Variance ; Aortic Diseases - metabolism ; Atherosclerosis (general aspects, experimental research) ; Basic Science ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cells, Cultured ; Collagen Type I - metabolism ; Collagenases ; Coronary Artery Disease - metabolism ; Endothelial Cells - metabolism ; Gelatinases - antagonists & inhibitors ; Gelatinases - metabolism ; Humans ; Matrix Metalloproteinase Inhibitors ; Medical sciences ; Membrane Proteins - antagonists & inhibitors ; Membrane Proteins - metabolism ; Middle Aged ; Muscle, Smooth, Vascular - metabolism ; Plaque, Atherosclerotic - metabolism ; Serine Endopeptidases - metabolism ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>European heart journal, 2011-11, Vol.32 (21), p.2713-2722</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2011. For permissions please email: journals.permissions@oup.com 2011</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c527t-e35f3ee1af8f3dd7475128cd83469471f0b898e5505a40d57724c781d8d4954f3</citedby><cites>FETCH-LOGICAL-c527t-e35f3ee1af8f3dd7475128cd83469471f0b898e5505a40d57724c781d8d4954f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,1578,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24637589$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21292680$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brokopp, Chad E.</creatorcontrib><creatorcontrib>Schoenauer, Roman</creatorcontrib><creatorcontrib>Richards, Peter</creatorcontrib><creatorcontrib>Bauer, Stefan</creatorcontrib><creatorcontrib>Lohmann, Christine</creatorcontrib><creatorcontrib>Emmert, Maximilian Y.</creatorcontrib><creatorcontrib>Weber, Benedikt</creatorcontrib><creatorcontrib>Winnik, Stephan</creatorcontrib><creatorcontrib>Aikawa, Elena</creatorcontrib><creatorcontrib>Graves, Kirk</creatorcontrib><creatorcontrib>Genoni, Michele</creatorcontrib><creatorcontrib>Vogt, Peter</creatorcontrib><creatorcontrib>Lüscher, Thomas F.</creatorcontrib><creatorcontrib>Renner, Christoph</creatorcontrib><creatorcontrib>Hoerstrup, Simon P.</creatorcontrib><creatorcontrib>Matter, Christian M.</creatorcontrib><title>Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description><![CDATA[Aims
Collagen degradation in atherosclerotic plaques with thin fibrous caps renders them more prone to rupture. Fibroblast activation protein (FAP) plays a role in arthritis and tumour formation through its collagenase activity. However, the significance of FAP in thin-cap human fibroatheromata remains unknown.
Methods and results
We detected enhanced FAP expression in type IV-V human aortic atheromata (n = 12), compared with type II-III lesions (n = 9; P < 0.01) and healthy aortae (n = 8; P < 0.01) by immunostaining and western blot analyses. Fibroblast activation protein was also increased in thin-cap (<65 µm) vs. thick-cap (≥65 µm) human coronary fibroatheromata (n = 12; P < 0.01). Fibroblast activation protein was expressed by human aortic smooth muscle cells (HASMC) as shown by colocalization on immunofluorescent aortic plaque stainings (n = 10; P < 0.01) and by flow cytometry in cell culture. Although macrophages did not express FAP, macrophage burden in human aortic plaques correlated with FAP expression (n = 12; R
2= 0.763; P < 0.05). Enzyme-linked immunosorbent assays showed a time- and dose-dependent up-regulation of FAP in response to human tumour necrosis factor α (TNFα) in HASMC (n = 6; P < 0.01). Moreover, supernatants from peripheral blood-derived macrophages induced FAP expression in cultured HASMC (n = 6; P < 0.01), an effect abolished by blocking TNFα (n = 6; P < 0.01). Fibroblast activation protein associated with collagen-poor regions in human coronary fibrous caps and digested type I collagen and gelatin in vitro (n = 6; P < 0.01). Zymography revealed that FAP-mediated collagenase activity was neutralized by an antibody directed against the FAP catalytic domain both in HASMC (n = 6; P < 0.01) and in fibrous caps of atherosclerotic plaques (n = 10; P < 0.01).
Conclusion
Fibroblast activation protein expression in HASMC is induced by macrophage-derived TNFα. Fibroblast activation protein associates with thin-cap human coronary fibroatheromata and contributes to type I collagen breakdown in fibrous caps.]]></description><subject>Adult</subject><subject>Aged</subject><subject>Analysis of Variance</subject><subject>Aortic Diseases - metabolism</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Basic Science</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Collagen Type I - metabolism</subject><subject>Collagenases</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Endothelial Cells - metabolism</subject><subject>Gelatinases - antagonists & inhibitors</subject><subject>Gelatinases - metabolism</subject><subject>Humans</subject><subject>Matrix Metalloproteinase Inhibitors</subject><subject>Medical sciences</subject><subject>Membrane Proteins - antagonists & inhibitors</subject><subject>Membrane Proteins - metabolism</subject><subject>Middle Aged</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Plaque, Atherosclerotic - metabolism</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><sourceid>EIF</sourceid><recordid>eNqFkcGL1DAUxoMo7uzq3ZPkIh6WuknatMlFkMXVhQUvCt7Ca_I6zdJpOkm6MP-9HTqOevL0Au_3fd8LHyFvOPvAmS5vcI49QsyPN9jvJdfPyIZLIQpdV_I52TCuZVHX6ucFuUzpkTGmal6_JBeCCy1qxTZkf-fbGNoBUqZgs3-C7MNIpxgy-pH6RP3oZouOtofl2Q2w260IjI463EZwmGg-TEjvqQ3DAFtcdCPNvR8LCxPtjgmQe4xhkcIr8qKDIeHr07wiP-4-f7_9Wjx8-3J_--mhsFI0ucBSdiUih051pXNN1UgulHWqrGpdNbxjrdIKpWQSKuZk04jKNoo75Sotq668Ih9X32lud-gsjjnCYKbodxAPJoA3_25G35tteDKlYLJq9GLw_mQQw37GlM3OJ4vLD0cMczKaCaaaBVxItpI2hpQiducUzsyxKHMuyqxFLZK3f193FvxuZgHenQBIFoYuwmh9-sNVddlIdTS6XrkwT_-P_QVLMbFn</recordid><startdate>20111101</startdate><enddate>20111101</enddate><creator>Brokopp, Chad E.</creator><creator>Schoenauer, Roman</creator><creator>Richards, Peter</creator><creator>Bauer, Stefan</creator><creator>Lohmann, Christine</creator><creator>Emmert, Maximilian Y.</creator><creator>Weber, Benedikt</creator><creator>Winnik, Stephan</creator><creator>Aikawa, Elena</creator><creator>Graves, Kirk</creator><creator>Genoni, Michele</creator><creator>Vogt, Peter</creator><creator>Lüscher, Thomas F.</creator><creator>Renner, Christoph</creator><creator>Hoerstrup, Simon P.</creator><creator>Matter, Christian M.</creator><general>Oxford University Press</general><scope>TOX</scope><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20111101</creationdate><title>Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata</title><author>Brokopp, Chad E. ; Schoenauer, Roman ; Richards, Peter ; Bauer, Stefan ; Lohmann, Christine ; Emmert, Maximilian Y. ; Weber, Benedikt ; Winnik, Stephan ; Aikawa, Elena ; Graves, Kirk ; Genoni, Michele ; Vogt, Peter ; Lüscher, Thomas F. ; Renner, Christoph ; Hoerstrup, Simon P. ; Matter, Christian M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c527t-e35f3ee1af8f3dd7475128cd83469471f0b898e5505a40d57724c781d8d4954f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Analysis of Variance</topic><topic>Aortic Diseases - metabolism</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Basic Science</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Collagen Type I - metabolism</topic><topic>Collagenases</topic><topic>Coronary Artery Disease - metabolism</topic><topic>Endothelial Cells - metabolism</topic><topic>Gelatinases - antagonists & inhibitors</topic><topic>Gelatinases - metabolism</topic><topic>Humans</topic><topic>Matrix Metalloproteinase Inhibitors</topic><topic>Medical sciences</topic><topic>Membrane Proteins - antagonists & inhibitors</topic><topic>Membrane Proteins - metabolism</topic><topic>Middle Aged</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Plaque, Atherosclerotic - metabolism</topic><topic>Serine Endopeptidases - metabolism</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brokopp, Chad E.</creatorcontrib><creatorcontrib>Schoenauer, Roman</creatorcontrib><creatorcontrib>Richards, Peter</creatorcontrib><creatorcontrib>Bauer, Stefan</creatorcontrib><creatorcontrib>Lohmann, Christine</creatorcontrib><creatorcontrib>Emmert, Maximilian Y.</creatorcontrib><creatorcontrib>Weber, Benedikt</creatorcontrib><creatorcontrib>Winnik, Stephan</creatorcontrib><creatorcontrib>Aikawa, Elena</creatorcontrib><creatorcontrib>Graves, Kirk</creatorcontrib><creatorcontrib>Genoni, Michele</creatorcontrib><creatorcontrib>Vogt, Peter</creatorcontrib><creatorcontrib>Lüscher, Thomas F.</creatorcontrib><creatorcontrib>Renner, Christoph</creatorcontrib><creatorcontrib>Hoerstrup, Simon P.</creatorcontrib><creatorcontrib>Matter, Christian M.</creatorcontrib><collection>Oxford Journals Open Access Collection</collection><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><collection>PubMed Central (Full Participant titles)</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brokopp, Chad E.</au><au>Schoenauer, Roman</au><au>Richards, Peter</au><au>Bauer, Stefan</au><au>Lohmann, Christine</au><au>Emmert, Maximilian Y.</au><au>Weber, Benedikt</au><au>Winnik, Stephan</au><au>Aikawa, Elena</au><au>Graves, Kirk</au><au>Genoni, Michele</au><au>Vogt, Peter</au><au>Lüscher, Thomas F.</au><au>Renner, Christoph</au><au>Hoerstrup, Simon P.</au><au>Matter, Christian M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2011-11-01</date><risdate>2011</risdate><volume>32</volume><issue>21</issue><spage>2713</spage><epage>2722</epage><pages>2713-2722</pages><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract><![CDATA[Aims
Collagen degradation in atherosclerotic plaques with thin fibrous caps renders them more prone to rupture. Fibroblast activation protein (FAP) plays a role in arthritis and tumour formation through its collagenase activity. However, the significance of FAP in thin-cap human fibroatheromata remains unknown.
Methods and results
We detected enhanced FAP expression in type IV-V human aortic atheromata (n = 12), compared with type II-III lesions (n = 9; P < 0.01) and healthy aortae (n = 8; P < 0.01) by immunostaining and western blot analyses. Fibroblast activation protein was also increased in thin-cap (<65 µm) vs. thick-cap (≥65 µm) human coronary fibroatheromata (n = 12; P < 0.01). Fibroblast activation protein was expressed by human aortic smooth muscle cells (HASMC) as shown by colocalization on immunofluorescent aortic plaque stainings (n = 10; P < 0.01) and by flow cytometry in cell culture. Although macrophages did not express FAP, macrophage burden in human aortic plaques correlated with FAP expression (n = 12; R
2= 0.763; P < 0.05). Enzyme-linked immunosorbent assays showed a time- and dose-dependent up-regulation of FAP in response to human tumour necrosis factor α (TNFα) in HASMC (n = 6; P < 0.01). Moreover, supernatants from peripheral blood-derived macrophages induced FAP expression in cultured HASMC (n = 6; P < 0.01), an effect abolished by blocking TNFα (n = 6; P < 0.01). Fibroblast activation protein associated with collagen-poor regions in human coronary fibrous caps and digested type I collagen and gelatin in vitro (n = 6; P < 0.01). Zymography revealed that FAP-mediated collagenase activity was neutralized by an antibody directed against the FAP catalytic domain both in HASMC (n = 6; P < 0.01) and in fibrous caps of atherosclerotic plaques (n = 10; P < 0.01).
Conclusion
Fibroblast activation protein expression in HASMC is induced by macrophage-derived TNFα. Fibroblast activation protein associates with thin-cap human coronary fibroatheromata and contributes to type I collagen breakdown in fibrous caps.]]></abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>21292680</pmid><doi>10.1093/eurheartj/ehq519</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | European heart journal, 2011-11, Vol.32 (21), p.2713-2722 |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Aged Analysis of Variance Aortic Diseases - metabolism Atherosclerosis (general aspects, experimental research) Basic Science Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cells, Cultured Collagen Type I - metabolism Collagenases Coronary Artery Disease - metabolism Endothelial Cells - metabolism Gelatinases - antagonists & inhibitors Gelatinases - metabolism Humans Matrix Metalloproteinase Inhibitors Medical sciences Membrane Proteins - antagonists & inhibitors Membrane Proteins - metabolism Middle Aged Muscle, Smooth, Vascular - metabolism Plaque, Atherosclerotic - metabolism Serine Endopeptidases - metabolism Tumor Necrosis Factor-alpha - pharmacology |
| title | Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata |
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