Influence of matrix metalloproteinase-12 on fibrinogen level
Abstract In vitro studies have shown that matrix metalloproteinase-12 (MMP12) can degrade fibrinogen, a clotting factor whose level predicts risk of advanced atherosclerosis and myocardial infarction. In this study, we found that mean plasma fibrinogen level was approximately 10-fold higher in MMP12...
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| Veröffentlicht in: | Atherosclerosis 2012-02, Vol.220 (2), p.351-354 |
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| creator | Motterle, Anna Xiao, Qingzhong Kiechl, Stefan Pender, Sylvia L.F Morris, Gareth E Willeit, Johann Caulfield, Mark J Ye, Shu |
| description | Abstract In vitro studies have shown that matrix metalloproteinase-12 (MMP12) can degrade fibrinogen, a clotting factor whose level predicts risk of advanced atherosclerosis and myocardial infarction. In this study, we found that mean plasma fibrinogen level was approximately 10-fold higher in MMP12 knockout mice than wildtype mice ( p = 0.0006). Differential allelic expression analysis of human MMP12 gene polymorphism rs17368582 in human vascular tissues showed an allele-specific effect on MMP12 expression, with one allele (T) having 1.6 fold higher expression level than the other allele (C) ( p = 0.0006). In a population cohort, we found that individuals homozygous for the MMP12 low expression allele had higher plasma fibrinogen levels (2.95 mg/mL compared with 2.61 mg/mL in other individuals, p = 0.029) and increased risk of advanced atherosclerosis [odds ratio 6.3 (95% CI 1.9–20.8), p = 0.003] and myocardial infarction [hazard ratio 5.6 (95% CI 1.7–18.3), p = 0.005]. In summary, our study in mouse and humans provides in vivo evidence of an effect of MMP12 on fibrinogen level. |
| doi_str_mv | 10.1016/j.atherosclerosis.2011.11.003 |
| format | Article |
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In this study, we found that mean plasma fibrinogen level was approximately 10-fold higher in MMP12 knockout mice than wildtype mice ( p = 0.0006). Differential allelic expression analysis of human MMP12 gene polymorphism rs17368582 in human vascular tissues showed an allele-specific effect on MMP12 expression, with one allele (T) having 1.6 fold higher expression level than the other allele (C) ( p = 0.0006). In a population cohort, we found that individuals homozygous for the MMP12 low expression allele had higher plasma fibrinogen levels (2.95 mg/mL compared with 2.61 mg/mL in other individuals, p = 0.029) and increased risk of advanced atherosclerosis [odds ratio 6.3 (95% CI 1.9–20.8), p = 0.003] and myocardial infarction [hazard ratio 5.6 (95% CI 1.7–18.3), p = 0.005]. In summary, our study in mouse and humans provides in vivo evidence of an effect of MMP12 on fibrinogen level.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2011.11.003</identifier><identifier>PMID: 22119538</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>alleles ; Animals ; Atherosclerosis ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - enzymology ; Atherosclerosis - genetics ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cardiovascular ; Coronary heart disease ; England ; Fibrinogen ; Fibrinogen - metabolism ; Gene Frequency ; genetic polymorphism ; Genetic Predisposition to Disease ; Heart ; homozygosity ; Homozygote ; Humans ; in vitro studies ; Italy ; Linear Models ; Linkage Disequilibrium ; Logistic Models ; Matrix Metalloproteinase 12 - deficiency ; Matrix Metalloproteinase 12 - genetics ; Matrix Metalloproteinase 12 - metabolism ; Matrix metalloproteinase-12 ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial infarction ; Myocardial Infarction - enzymology ; Myocardial Infarction - genetics ; Odds Ratio ; Phenotype ; Polymorphism, Single Nucleotide ; Proportional Hazards Models ; Prospective Studies ; risk ; Risk Assessment ; Risk Factors ; vascular tissues</subject><ispartof>Atherosclerosis, 2012-02, Vol.220 (2), p.351-354</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2011 Elsevier Ireland Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-60f238fc461c1906a63a6dde61341e7ca5d6dfa7ddcebd5f625ea03ade548e563</citedby><cites>FETCH-LOGICAL-c563t-60f238fc461c1906a63a6dde61341e7ca5d6dfa7ddcebd5f625ea03ade548e563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.atherosclerosis.2011.11.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25455002$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22119538$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Motterle, Anna</creatorcontrib><creatorcontrib>Xiao, Qingzhong</creatorcontrib><creatorcontrib>Kiechl, Stefan</creatorcontrib><creatorcontrib>Pender, Sylvia L.F</creatorcontrib><creatorcontrib>Morris, Gareth E</creatorcontrib><creatorcontrib>Willeit, Johann</creatorcontrib><creatorcontrib>Caulfield, Mark J</creatorcontrib><creatorcontrib>Ye, Shu</creatorcontrib><title>Influence of matrix metalloproteinase-12 on fibrinogen level</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Abstract In vitro studies have shown that matrix metalloproteinase-12 (MMP12) can degrade fibrinogen, a clotting factor whose level predicts risk of advanced atherosclerosis and myocardial infarction. In this study, we found that mean plasma fibrinogen level was approximately 10-fold higher in MMP12 knockout mice than wildtype mice ( p = 0.0006). Differential allelic expression analysis of human MMP12 gene polymorphism rs17368582 in human vascular tissues showed an allele-specific effect on MMP12 expression, with one allele (T) having 1.6 fold higher expression level than the other allele (C) ( p = 0.0006). In a population cohort, we found that individuals homozygous for the MMP12 low expression allele had higher plasma fibrinogen levels (2.95 mg/mL compared with 2.61 mg/mL in other individuals, p = 0.029) and increased risk of advanced atherosclerosis [odds ratio 6.3 (95% CI 1.9–20.8), p = 0.003] and myocardial infarction [hazard ratio 5.6 (95% CI 1.7–18.3), p = 0.005]. In summary, our study in mouse and humans provides in vivo evidence of an effect of MMP12 on fibrinogen level.</description><subject>alleles</subject><subject>Animals</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - enzymology</subject><subject>Atherosclerosis - genetics</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Coronary heart disease</subject><subject>England</subject><subject>Fibrinogen</subject><subject>Fibrinogen - metabolism</subject><subject>Gene Frequency</subject><subject>genetic polymorphism</subject><subject>Genetic Predisposition to Disease</subject><subject>Heart</subject><subject>homozygosity</subject><subject>Homozygote</subject><subject>Humans</subject><subject>in vitro studies</subject><subject>Italy</subject><subject>Linear Models</subject><subject>Linkage Disequilibrium</subject><subject>Logistic Models</subject><subject>Matrix Metalloproteinase 12 - deficiency</subject><subject>Matrix Metalloproteinase 12 - genetics</subject><subject>Matrix Metalloproteinase 12 - metabolism</subject><subject>Matrix metalloproteinase-12</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - enzymology</subject><subject>Myocardial Infarction - genetics</subject><subject>Odds Ratio</subject><subject>Phenotype</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Proportional Hazards Models</subject><subject>Prospective Studies</subject><subject>risk</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>vascular tissues</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk9v1DAQxS0EokvhK0AuFacsM0nsJBIgoYr-kSpxKD1bXntcvHjtYicV_fY47NJDT0gj-_KbN09vhrEThDUCig_btZp-UIpZ--V1ed0A4roUQPuMrXDoxxq7oXvOVgAN1iNyOGKvct4CQNfj8JIdNQ3iyNthxT5eButnCpqqaKudmpL7Xe1oUt7HuxQnckFlqrGpYqis2yQX4i2FytM9-dfshVU-05vDf8xuzr5-P72or76dX55-uao1F-1UC7BNO1jdCdQ4glCiVcIYEth2SL1W3AhjVW-Mpo3hVjScFLTKEO8GKhLH7P1etzj6NVOe5M5lTd6rQHHOcsSe90MPTSE_7UldssmJrLxLbqfSg0SQS35yK5_kJ5f8ZKmSX-l_e5g0b3ZkHrv_BVaAkwOgslbeJhV00XjkeMc5_DXybs9ZFaW6TYW5uS6T-LKEoayhEOd7gkpy946SzNotizAukZ6kie6_TX9-oqS9C67Y-0kPlLdxTqGsR6LMjQR5vZzFchVYtKFvoP0D-zG2QQ</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Motterle, Anna</creator><creator>Xiao, Qingzhong</creator><creator>Kiechl, Stefan</creator><creator>Pender, Sylvia L.F</creator><creator>Morris, Gareth E</creator><creator>Willeit, Johann</creator><creator>Caulfield, Mark J</creator><creator>Ye, Shu</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>FBQ</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></search><sort><creationdate>20120201</creationdate><title>Influence of matrix metalloproteinase-12 on fibrinogen level</title><author>Motterle, Anna ; Xiao, Qingzhong ; Kiechl, Stefan ; Pender, Sylvia L.F ; Morris, Gareth E ; Willeit, Johann ; Caulfield, Mark J ; Ye, Shu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-60f238fc461c1906a63a6dde61341e7ca5d6dfa7ddcebd5f625ea03ade548e563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>alleles</topic><topic>Animals</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - enzymology</topic><topic>Atherosclerosis - genetics</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular</topic><topic>Coronary heart disease</topic><topic>England</topic><topic>Fibrinogen</topic><topic>Fibrinogen - metabolism</topic><topic>Gene Frequency</topic><topic>genetic polymorphism</topic><topic>Genetic Predisposition to Disease</topic><topic>Heart</topic><topic>homozygosity</topic><topic>Homozygote</topic><topic>Humans</topic><topic>in vitro studies</topic><topic>Italy</topic><topic>Linear Models</topic><topic>Linkage Disequilibrium</topic><topic>Logistic Models</topic><topic>Matrix Metalloproteinase 12 - deficiency</topic><topic>Matrix Metalloproteinase 12 - genetics</topic><topic>Matrix Metalloproteinase 12 - metabolism</topic><topic>Matrix metalloproteinase-12</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - enzymology</topic><topic>Myocardial Infarction - genetics</topic><topic>Odds Ratio</topic><topic>Phenotype</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Proportional Hazards Models</topic><topic>Prospective Studies</topic><topic>risk</topic><topic>Risk Assessment</topic><topic>Risk Factors</topic><topic>vascular tissues</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Motterle, Anna</creatorcontrib><creatorcontrib>Xiao, Qingzhong</creatorcontrib><creatorcontrib>Kiechl, Stefan</creatorcontrib><creatorcontrib>Pender, Sylvia L.F</creatorcontrib><creatorcontrib>Morris, Gareth E</creatorcontrib><creatorcontrib>Willeit, Johann</creatorcontrib><creatorcontrib>Caulfield, Mark J</creatorcontrib><creatorcontrib>Ye, Shu</creatorcontrib><collection>AGRIS</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><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Motterle, Anna</au><au>Xiao, Qingzhong</au><au>Kiechl, Stefan</au><au>Pender, Sylvia L.F</au><au>Morris, Gareth E</au><au>Willeit, Johann</au><au>Caulfield, Mark J</au><au>Ye, Shu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Influence of matrix metalloproteinase-12 on fibrinogen level</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>220</volume><issue>2</issue><spage>351</spage><epage>354</epage><pages>351-354</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Abstract In vitro studies have shown that matrix metalloproteinase-12 (MMP12) can degrade fibrinogen, a clotting factor whose level predicts risk of advanced atherosclerosis and myocardial infarction. In this study, we found that mean plasma fibrinogen level was approximately 10-fold higher in MMP12 knockout mice than wildtype mice ( p = 0.0006). Differential allelic expression analysis of human MMP12 gene polymorphism rs17368582 in human vascular tissues showed an allele-specific effect on MMP12 expression, with one allele (T) having 1.6 fold higher expression level than the other allele (C) ( p = 0.0006). In a population cohort, we found that individuals homozygous for the MMP12 low expression allele had higher plasma fibrinogen levels (2.95 mg/mL compared with 2.61 mg/mL in other individuals, p = 0.029) and increased risk of advanced atherosclerosis [odds ratio 6.3 (95% CI 1.9–20.8), p = 0.003] and myocardial infarction [hazard ratio 5.6 (95% CI 1.7–18.3), p = 0.005]. In summary, our study in mouse and humans provides in vivo evidence of an effect of MMP12 on fibrinogen level.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>22119538</pmid><doi>10.1016/j.atherosclerosis.2011.11.003</doi><tpages>4</tpages></addata></record> |
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| subjects | alleles Animals Atherosclerosis Atherosclerosis (general aspects, experimental research) Atherosclerosis - enzymology Atherosclerosis - genetics Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiovascular Coronary heart disease England Fibrinogen Fibrinogen - metabolism Gene Frequency genetic polymorphism Genetic Predisposition to Disease Heart homozygosity Homozygote Humans in vitro studies Italy Linear Models Linkage Disequilibrium Logistic Models Matrix Metalloproteinase 12 - deficiency Matrix Metalloproteinase 12 - genetics Matrix Metalloproteinase 12 - metabolism Matrix metalloproteinase-12 Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Myocardial infarction Myocardial Infarction - enzymology Myocardial Infarction - genetics Odds Ratio Phenotype Polymorphism, Single Nucleotide Proportional Hazards Models Prospective Studies risk Risk Assessment Risk Factors vascular tissues |
| title | Influence of matrix metalloproteinase-12 on fibrinogen level |
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