Stromelysin promoter 5A/6A polymorphism is associated with acute myocardial infarction
Rupture of the fibrous cap of an atherosclerotic plaque is a key event that predisposes to acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) may contribute to weakening of the cap, which favors rupture. Stromelysin, a member of MMP family, is identified extensively in human coronar...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1999-06, Vol.99 (21), p.2717-2719 |
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| container_title | Circulation (New York, N.Y.) |
| container_volume | 99 |
| creator | Terashima, M Akita, H Kanazawa, K Inoue, N Yamada, S Ito, K Matsuda, Y Takai, E Iwai, C Kurogane, H Yoshida, Y Yokoyama, M |
| description | Rupture of the fibrous cap of an atherosclerotic plaque is a key event that predisposes to acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) may contribute to weakening of the cap, which favors rupture. Stromelysin, a member of MMP family, is identified extensively in human coronary atherosclerotic lesions. It can degrade most of the constituents of extracellular matrix as well as activating other MMPs, which suggests that it may play an important role in plaque rupture. Recently, a common variant (5A/6A) in the promoter of the stromelysin gene has been identified. The 5A/6A polymorphism could regulate the transcription of the stromelysin gene in an allele-specific manner.
To investigate the relation between the 5A/6A polymorphism in the promoter of the stromelysin gene and AMI, we conducted a case-control study of 330 AMI patients and 330 control subjects. The prevalence of the 5A/6A+5A/5A genotype was significantly more frequent in the patients with AMI than in control subjects (48.8% vs 32.7%, P |
| doi_str_mv | 10.1161/01.CIR.99.21.2717 |
| format | Article |
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To investigate the relation between the 5A/6A polymorphism in the promoter of the stromelysin gene and AMI, we conducted a case-control study of 330 AMI patients and 330 control subjects. The prevalence of the 5A/6A+5A/5A genotype was significantly more frequent in the patients with AMI than in control subjects (48.8% vs 32.7%, P<0.0001). In logistic regression models, the odds ratio of the 5A/6A+5A/5A was 2.25 (95% CI, 1.51 to 3.35). The association of 5A/6A polymorphism with AMI was statistically significant and independent of other risk factors.
The 5A/6A polymorphism in the promoter of the stromelysin gene is a novel pathogenetic risk factor for AMI.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.99.21.2717</identifier><identifier>PMID: 10351963</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Alleles ; Case-Control Studies ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Logistic Models ; Male ; Matrix Metalloproteinase 3 - genetics ; Middle Aged ; Myocardial Infarction - genetics ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Regression Analysis ; Risk Factors ; Rupture</subject><ispartof>Circulation (New York, N.Y.), 1999-06, Vol.99 (21), p.2717-2719</ispartof><rights>Copyright American Heart Association, Inc. Jun 1, 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c409t-d50956383003542dbef4d6fb4a9db7c2dfd7a2199912314b62a6d613ec192b683</citedby><cites>FETCH-LOGICAL-c409t-d50956383003542dbef4d6fb4a9db7c2dfd7a2199912314b62a6d613ec192b683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10351963$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Terashima, M</creatorcontrib><creatorcontrib>Akita, H</creatorcontrib><creatorcontrib>Kanazawa, K</creatorcontrib><creatorcontrib>Inoue, N</creatorcontrib><creatorcontrib>Yamada, S</creatorcontrib><creatorcontrib>Ito, K</creatorcontrib><creatorcontrib>Matsuda, Y</creatorcontrib><creatorcontrib>Takai, E</creatorcontrib><creatorcontrib>Iwai, C</creatorcontrib><creatorcontrib>Kurogane, H</creatorcontrib><creatorcontrib>Yoshida, Y</creatorcontrib><creatorcontrib>Yokoyama, M</creatorcontrib><title>Stromelysin promoter 5A/6A polymorphism is associated with acute myocardial infarction</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Rupture of the fibrous cap of an atherosclerotic plaque is a key event that predisposes to acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) may contribute to weakening of the cap, which favors rupture. Stromelysin, a member of MMP family, is identified extensively in human coronary atherosclerotic lesions. It can degrade most of the constituents of extracellular matrix as well as activating other MMPs, which suggests that it may play an important role in plaque rupture. Recently, a common variant (5A/6A) in the promoter of the stromelysin gene has been identified. The 5A/6A polymorphism could regulate the transcription of the stromelysin gene in an allele-specific manner.
To investigate the relation between the 5A/6A polymorphism in the promoter of the stromelysin gene and AMI, we conducted a case-control study of 330 AMI patients and 330 control subjects. The prevalence of the 5A/6A+5A/5A genotype was significantly more frequent in the patients with AMI than in control subjects (48.8% vs 32.7%, P<0.0001). In logistic regression models, the odds ratio of the 5A/6A+5A/5A was 2.25 (95% CI, 1.51 to 3.35). The association of 5A/6A polymorphism with AMI was statistically significant and independent of other risk factors.
The 5A/6A polymorphism in the promoter of the stromelysin gene is a novel pathogenetic risk factor for AMI.</description><subject>Alleles</subject><subject>Case-Control Studies</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Matrix Metalloproteinase 3 - genetics</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - genetics</subject><subject>Polymorphism, Genetic</subject><subject>Promoter Regions, Genetic</subject><subject>Regression Analysis</subject><subject>Risk Factors</subject><subject>Rupture</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkMFq3DAQhkVJyW7TPEAvQeSQmx2NZEmr47Ik6UKg0CS9ClmSiRbb2kg2xW8fhc2h9DQz8P3Dz4fQDyA1gIBbAvVu_7tWqqZQUwnyC1oDp03VcKbO0JoQoirJKF2hbzkfyimY5OdoBYRxUIKt0Z-nKcXB90sOIz6WNU4-Yb69FVt8jP0yxHR8DXnAIWOTc7TBTN7hv2F6xcbOk8fDEq1JLpgeh7EzyU4hjt_R18702V9-zgv0cn_3vPtZPf562O-2j5VtiJoqx4nigm0YKYUa6lrfNU50bWOUa6WlrnPSUFBKAWXQtIIa4QQwb0HRVmzYBbo5_S3V32afJz2EbH3fm9HHOWuhpJJ8Iwp4_R94iHMaSzdNgcqGg4QCwQmyKeacfKePKQwmLRqI_jCuCehiXCtVUvrDeMlcfT6e28G7fxInxewdAcd71g</recordid><startdate>19990601</startdate><enddate>19990601</enddate><creator>Terashima, M</creator><creator>Akita, H</creator><creator>Kanazawa, K</creator><creator>Inoue, N</creator><creator>Yamada, S</creator><creator>Ito, K</creator><creator>Matsuda, Y</creator><creator>Takai, E</creator><creator>Iwai, C</creator><creator>Kurogane, H</creator><creator>Yoshida, Y</creator><creator>Yokoyama, M</creator><general>American Heart Association, Inc</general><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>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19990601</creationdate><title>Stromelysin promoter 5A/6A polymorphism is associated with acute myocardial infarction</title><author>Terashima, M ; Akita, H ; Kanazawa, K ; Inoue, N ; Yamada, S ; Ito, K ; Matsuda, Y ; Takai, E ; Iwai, C ; Kurogane, H ; Yoshida, Y ; Yokoyama, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c409t-d50956383003542dbef4d6fb4a9db7c2dfd7a2199912314b62a6d613ec192b683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Alleles</topic><topic>Case-Control Studies</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Matrix Metalloproteinase 3 - genetics</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - genetics</topic><topic>Polymorphism, Genetic</topic><topic>Promoter Regions, Genetic</topic><topic>Regression Analysis</topic><topic>Risk Factors</topic><topic>Rupture</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Terashima, M</creatorcontrib><creatorcontrib>Akita, H</creatorcontrib><creatorcontrib>Kanazawa, K</creatorcontrib><creatorcontrib>Inoue, N</creatorcontrib><creatorcontrib>Yamada, S</creatorcontrib><creatorcontrib>Ito, K</creatorcontrib><creatorcontrib>Matsuda, Y</creatorcontrib><creatorcontrib>Takai, E</creatorcontrib><creatorcontrib>Iwai, C</creatorcontrib><creatorcontrib>Kurogane, H</creatorcontrib><creatorcontrib>Yoshida, Y</creatorcontrib><creatorcontrib>Yokoyama, M</creatorcontrib><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>Nursing & Allied Health Premium</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>Terashima, M</au><au>Akita, H</au><au>Kanazawa, K</au><au>Inoue, N</au><au>Yamada, S</au><au>Ito, K</au><au>Matsuda, Y</au><au>Takai, E</au><au>Iwai, C</au><au>Kurogane, H</au><au>Yoshida, Y</au><au>Yokoyama, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stromelysin promoter 5A/6A polymorphism is associated with acute myocardial infarction</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1999-06-01</date><risdate>1999</risdate><volume>99</volume><issue>21</issue><spage>2717</spage><epage>2719</epage><pages>2717-2719</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Rupture of the fibrous cap of an atherosclerotic plaque is a key event that predisposes to acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) may contribute to weakening of the cap, which favors rupture. Stromelysin, a member of MMP family, is identified extensively in human coronary atherosclerotic lesions. It can degrade most of the constituents of extracellular matrix as well as activating other MMPs, which suggests that it may play an important role in plaque rupture. Recently, a common variant (5A/6A) in the promoter of the stromelysin gene has been identified. The 5A/6A polymorphism could regulate the transcription of the stromelysin gene in an allele-specific manner.
To investigate the relation between the 5A/6A polymorphism in the promoter of the stromelysin gene and AMI, we conducted a case-control study of 330 AMI patients and 330 control subjects. The prevalence of the 5A/6A+5A/5A genotype was significantly more frequent in the patients with AMI than in control subjects (48.8% vs 32.7%, P<0.0001). In logistic regression models, the odds ratio of the 5A/6A+5A/5A was 2.25 (95% CI, 1.51 to 3.35). The association of 5A/6A polymorphism with AMI was statistically significant and independent of other risk factors.
The 5A/6A polymorphism in the promoter of the stromelysin gene is a novel pathogenetic risk factor for AMI.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>10351963</pmid><doi>10.1161/01.CIR.99.21.2717</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 1999-06, Vol.99 (21), p.2717-2719 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Alleles Case-Control Studies Female Genetic Predisposition to Disease Genotype Humans Logistic Models Male Matrix Metalloproteinase 3 - genetics Middle Aged Myocardial Infarction - genetics Polymorphism, Genetic Promoter Regions, Genetic Regression Analysis Risk Factors Rupture |
| title | Stromelysin promoter 5A/6A polymorphism is associated with acute myocardial infarction |
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