Tumor necrosis factor receptor 2 gene (TNFRSF1B) in genetic basis of coronary artery disease
Tumor necrosis factor (TNF)-alpha has been implicated in pathophysiological processes in coronary artery disease (CAD). TNF receptor 2 is of particular interest in mediating such effects. The gene for this receptor (TNF-RSF1B) has, moreover, been implicated in hypertension, elevated cholesterol and...
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| Veröffentlicht in: | Journal of molecular medicine (Berlin, Germany) Germany), 2001-04, Vol.79 (2-3), p.109-115 |
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| creator | BENJAFIELD, Adam V XING LI WANG MORRIS, Brian J |
| description | Tumor necrosis factor (TNF)-alpha has been implicated in pathophysiological processes in coronary artery disease (CAD). TNF receptor 2 is of particular interest in mediating such effects. The gene for this receptor (TNF-RSF1B) has, moreover, been implicated in hypertension, elevated cholesterol and insulin resistance. TNFRSF1B is thus a worthy candidate in studies of the genetic basis of CAD. We therefore conducted a case-control study of a microsatellite marker with five alleles (CA13-CA17) in intron 4 of TNFRSF1B in 1006 well-characterized white patients with angiographically confirmed CAD and a control group of 183 healthy subjects. We found a strong association of the TNFRSF1B marker with CAD (chi2=40, P=0.00000069). The frequency of the CA16 allele was 33% in CAD vs. 21% in control (odds ratio, OR, to have CAD for presence vs. absence of CA16 allele in CA16 homozygotes was 4.5, 95% CI 2.1-9.4, P |
| doi_str_mv | 10.1007/s001090000168 |
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TNF receptor 2 is of particular interest in mediating such effects. The gene for this receptor (TNF-RSF1B) has, moreover, been implicated in hypertension, elevated cholesterol and insulin resistance. TNFRSF1B is thus a worthy candidate in studies of the genetic basis of CAD. We therefore conducted a case-control study of a microsatellite marker with five alleles (CA13-CA17) in intron 4 of TNFRSF1B in 1006 well-characterized white patients with angiographically confirmed CAD and a control group of 183 healthy subjects. We found a strong association of the TNFRSF1B marker with CAD (chi2=40, P=0.00000069). The frequency of the CA16 allele was 33% in CAD vs. 21% in control (odds ratio, OR, to have CAD for presence vs. absence of CA16 allele in CA16 homozygotes was 4.5, 95% CI 2.1-9.4, P<0.0001; in CA16 heterozygotes OR was 1.3, 95% CI 0.94-1.89, P=0.10). The frequency of the major allele (CA15) was 43% in CAD vs. 56% in controls (in CA15 homozygotes OR 0.33, 95% CI 0.20-0.52, P<0.0001; in heterozygotes OR 0.41, 95% CI 0.26-0.63, P<0.0001). In a stepwise logistic regression model the CA16 allele was significantly associated with overweight (OR 1.44, 95% CI 1.0-1.9, P=0.027). Apolipoprotein A-I was elevated (P<0.0001), as was high-density lipoprotein (P=0.098), and severity of angina was decreased (P=0.024) as a function of genotype. Plasma soluble (s) TNF-R2 was 5.1 +/- 0.1 ng/ml in CAD vs. 3.2 +/- 0.1 in control (P<0.0001), 5.2 +/- 0.1 in the presence vs. 4.6 +/- 0.2 in the absence of vessel disease (P=0.009), and rose with increasing severity of angina: 4.2 +/- 0.2 (no angina), 5.0 +/- 0.1 (stable angina), 5.4 +/- 0.2 (unstable angina; P=0.003). sTNF-R2 was correlated with age, cholesterol, creatinine, fibrinogen, transforming growth factor beta and homocysteine and was influenced by TNFRSF1B genotype. Thus genetic variation in or near the TNFRSF1B locus may predispose to CAD.</description><identifier>ISSN: 0946-2716</identifier><identifier>EISSN: 1432-1440</identifier><identifier>DOI: 10.1007/s001090000168</identifier><identifier>PMID: 11357933</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Adult ; Alleles ; Biological and medical sciences ; Cardiology. Vascular system ; Case-Control Studies ; Coronary Disease - etiology ; Coronary Disease - genetics ; Coronary heart disease ; Female ; Heart ; Humans ; Male ; Medical sciences ; Middle Aged ; Polymorphism, Genetic ; Receptors, Tumor Necrosis Factor - genetics ; Receptors, Tumor Necrosis Factor, Type II ; Risk Factors</subject><ispartof>Journal of molecular medicine (Berlin, Germany), 2001-04, Vol.79 (2-3), p.109-115</ispartof><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c318t-7a0debdffb3ddc0bd5001fba21641306e99fbe339d09e60f58bd7d4559df9db73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1013780$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11357933$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BENJAFIELD, Adam V</creatorcontrib><creatorcontrib>XING LI WANG</creatorcontrib><creatorcontrib>MORRIS, Brian J</creatorcontrib><title>Tumor necrosis factor receptor 2 gene (TNFRSF1B) in genetic basis of coronary artery disease</title><title>Journal of molecular medicine (Berlin, Germany)</title><addtitle>J Mol Med (Berl)</addtitle><description>Tumor necrosis factor (TNF)-alpha has been implicated in pathophysiological processes in coronary artery disease (CAD). TNF receptor 2 is of particular interest in mediating such effects. The gene for this receptor (TNF-RSF1B) has, moreover, been implicated in hypertension, elevated cholesterol and insulin resistance. TNFRSF1B is thus a worthy candidate in studies of the genetic basis of CAD. We therefore conducted a case-control study of a microsatellite marker with five alleles (CA13-CA17) in intron 4 of TNFRSF1B in 1006 well-characterized white patients with angiographically confirmed CAD and a control group of 183 healthy subjects. We found a strong association of the TNFRSF1B marker with CAD (chi2=40, P=0.00000069). The frequency of the CA16 allele was 33% in CAD vs. 21% in control (odds ratio, OR, to have CAD for presence vs. absence of CA16 allele in CA16 homozygotes was 4.5, 95% CI 2.1-9.4, P<0.0001; in CA16 heterozygotes OR was 1.3, 95% CI 0.94-1.89, P=0.10). The frequency of the major allele (CA15) was 43% in CAD vs. 56% in controls (in CA15 homozygotes OR 0.33, 95% CI 0.20-0.52, P<0.0001; in heterozygotes OR 0.41, 95% CI 0.26-0.63, P<0.0001). In a stepwise logistic regression model the CA16 allele was significantly associated with overweight (OR 1.44, 95% CI 1.0-1.9, P=0.027). Apolipoprotein A-I was elevated (P<0.0001), as was high-density lipoprotein (P=0.098), and severity of angina was decreased (P=0.024) as a function of genotype. Plasma soluble (s) TNF-R2 was 5.1 +/- 0.1 ng/ml in CAD vs. 3.2 +/- 0.1 in control (P<0.0001), 5.2 +/- 0.1 in the presence vs. 4.6 +/- 0.2 in the absence of vessel disease (P=0.009), and rose with increasing severity of angina: 4.2 +/- 0.2 (no angina), 5.0 +/- 0.1 (stable angina), 5.4 +/- 0.2 (unstable angina; P=0.003). sTNF-R2 was correlated with age, cholesterol, creatinine, fibrinogen, transforming growth factor beta and homocysteine and was influenced by TNFRSF1B genotype. Thus genetic variation in or near the TNFRSF1B locus may predispose to CAD.</description><subject>Adult</subject><subject>Alleles</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Coronary Disease - etiology</subject><subject>Coronary Disease - genetics</subject><subject>Coronary heart disease</subject><subject>Female</subject><subject>Heart</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Polymorphism, Genetic</subject><subject>Receptors, Tumor Necrosis Factor - genetics</subject><subject>Receptors, Tumor Necrosis Factor, Type II</subject><subject>Risk Factors</subject><issn>0946-2716</issn><issn>1432-1440</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkE1LxDAQhoMo7rp69Co9iOihOmnapjnq4qqwKOh6E0o-JlLptmvSHvz3pm5Bnct88MzLzEvIMYVLCsCvPAAFASFoXuyQKU1ZEtM0hV0yBZHmccJpPiEH3n8EhGci3ScTSlnGBWNT8rbq162LGtSu9ZWPrNRd6B1q3AxFEr1jg9H56nHx_LKgNxdR1fyMukpHSg4rrY1069pGuq9Iug5DMpVH6fGQ7FlZezwa84y8Lm5X8_t4-XT3ML9exprRoou5BIPKWKuYMRqUycKlVsmE5illkKMQViFjwoDAHGxWKMNNmmXCWGEUZzNyttXduPazR9-V68prrGvZYNv7kkOR5gWHAMZbcPjWO7TlxlXrcHhJoRzsLP_ZGfiTUbhXazS_9OhfAE5HQHota-tkoyv_R5UyXgD7BpitfCg</recordid><startdate>20010401</startdate><enddate>20010401</enddate><creator>BENJAFIELD, Adam V</creator><creator>XING LI WANG</creator><creator>MORRIS, Brian J</creator><general>Springer</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>7X8</scope></search><sort><creationdate>20010401</creationdate><title>Tumor necrosis factor receptor 2 gene (TNFRSF1B) in genetic basis of coronary artery disease</title><author>BENJAFIELD, Adam V ; XING LI WANG ; MORRIS, Brian J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c318t-7a0debdffb3ddc0bd5001fba21641306e99fbe339d09e60f58bd7d4559df9db73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Coronary Disease - etiology</topic><topic>Coronary Disease - genetics</topic><topic>Coronary heart disease</topic><topic>Female</topic><topic>Heart</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Polymorphism, Genetic</topic><topic>Receptors, Tumor Necrosis Factor - genetics</topic><topic>Receptors, Tumor Necrosis Factor, Type II</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BENJAFIELD, Adam V</creatorcontrib><creatorcontrib>XING LI WANG</creatorcontrib><creatorcontrib>MORRIS, Brian 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>MEDLINE - Academic</collection><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BENJAFIELD, Adam V</au><au>XING LI WANG</au><au>MORRIS, Brian J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor necrosis factor receptor 2 gene (TNFRSF1B) in genetic basis of coronary artery disease</atitle><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle><addtitle>J Mol Med (Berl)</addtitle><date>2001-04-01</date><risdate>2001</risdate><volume>79</volume><issue>2-3</issue><spage>109</spage><epage>115</epage><pages>109-115</pages><issn>0946-2716</issn><eissn>1432-1440</eissn><abstract>Tumor necrosis factor (TNF)-alpha has been implicated in pathophysiological processes in coronary artery disease (CAD). TNF receptor 2 is of particular interest in mediating such effects. The gene for this receptor (TNF-RSF1B) has, moreover, been implicated in hypertension, elevated cholesterol and insulin resistance. TNFRSF1B is thus a worthy candidate in studies of the genetic basis of CAD. We therefore conducted a case-control study of a microsatellite marker with five alleles (CA13-CA17) in intron 4 of TNFRSF1B in 1006 well-characterized white patients with angiographically confirmed CAD and a control group of 183 healthy subjects. We found a strong association of the TNFRSF1B marker with CAD (chi2=40, P=0.00000069). The frequency of the CA16 allele was 33% in CAD vs. 21% in control (odds ratio, OR, to have CAD for presence vs. absence of CA16 allele in CA16 homozygotes was 4.5, 95% CI 2.1-9.4, P<0.0001; in CA16 heterozygotes OR was 1.3, 95% CI 0.94-1.89, P=0.10). The frequency of the major allele (CA15) was 43% in CAD vs. 56% in controls (in CA15 homozygotes OR 0.33, 95% CI 0.20-0.52, P<0.0001; in heterozygotes OR 0.41, 95% CI 0.26-0.63, P<0.0001). In a stepwise logistic regression model the CA16 allele was significantly associated with overweight (OR 1.44, 95% CI 1.0-1.9, P=0.027). Apolipoprotein A-I was elevated (P<0.0001), as was high-density lipoprotein (P=0.098), and severity of angina was decreased (P=0.024) as a function of genotype. Plasma soluble (s) TNF-R2 was 5.1 +/- 0.1 ng/ml in CAD vs. 3.2 +/- 0.1 in control (P<0.0001), 5.2 +/- 0.1 in the presence vs. 4.6 +/- 0.2 in the absence of vessel disease (P=0.009), and rose with increasing severity of angina: 4.2 +/- 0.2 (no angina), 5.0 +/- 0.1 (stable angina), 5.4 +/- 0.2 (unstable angina; P=0.003). sTNF-R2 was correlated with age, cholesterol, creatinine, fibrinogen, transforming growth factor beta and homocysteine and was influenced by TNFRSF1B genotype. Thus genetic variation in or near the TNFRSF1B locus may predispose to CAD.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>11357933</pmid><doi>10.1007/s001090000168</doi><tpages>7</tpages></addata></record> |
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| subjects | Adult Alleles Biological and medical sciences Cardiology. Vascular system Case-Control Studies Coronary Disease - etiology Coronary Disease - genetics Coronary heart disease Female Heart Humans Male Medical sciences Middle Aged Polymorphism, Genetic Receptors, Tumor Necrosis Factor - genetics Receptors, Tumor Necrosis Factor, Type II Risk Factors |
| title | Tumor necrosis factor receptor 2 gene (TNFRSF1B) in genetic basis of coronary artery disease |
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