Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Tumor necrosis factor receptor 2 gene (TNFRSF1B) in genetic basis of coronary artery disease
Autore:
Benjafield, AV; Wang, XL; Morris, BJ;
Indirizzi:
Univ Sydney, Dept Physiol, Basic & Clin Genom Lab, Sydney, NSW 2006, Australia Univ Sydney Sydney NSW Australia 2006 om Lab, Sydney, NSW 2006, Australia Univ Sydney, Biomed Res Inst, Sydney, NSW 2006, Australia Univ Sydney Sydney NSW Australia 2006 s Inst, Sydney, NSW 2006, Australia Univ New S Wales, Prince Wales Hosp, Ctr Thrombosis & Vasc Res, CardiovascGenet Lab, Sydney, NSW, Australia Univ New S Wales Sydney NSW Australia cGenet Lab, Sydney, NSW, Australia SW Fdn Biomed Res, Dept Genet, San Antonio, TX 78245 USA SW Fdn Biomed Res San Antonio TX USA 78245 net, San Antonio, TX 78245 USA
Titolo Testata:
JOURNAL OF MOLECULAR MEDICINE-JMM
fascicolo: 2-3, volume: 79, anno: 2001,
pagine: 109 - 115
SICI:
0946-2716(200104)79:2-3<109:TNFR2G>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED INSULIN-RESISTANCE; FACTOR-ALPHA; TNF RECEPTOR; KEY COMPONENT; HEART-DISEASE; UP-REGULATION; GROWTH-FACTOR; A-I; OBESITY; CYTOKINES;
Keywords:
tumor necrosis factor receptor; tumor necrosis factor receptor superfamily member 1B gene; coronary artery disease; genetic polymorphism; case-control study;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Morris, BJ Univ Sydney, Dept Physiol, Basic & Clin Genom Lab, Bldg F13, Sydney, NSW 2006, Australia Univ Sydney Bldg F13 Sydney NSW Australia 2006 2006, Australia
Citazione:
A.V. Benjafield et al., "Tumor necrosis factor receptor 2 gene (TNFRSF1B) in genetic basis of coronary artery disease", J MOL MED-J, 79(2-3), 2001, pp. 109-115

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-RSFIB) has, moreover, been implicated in hypertension, elevated cholesterol andinsulin resistance. TNFRSFIB 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 TNFRSFIB 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 TNFRSFIB marker with CAD (chi (2)=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; inheterozygotes 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<plus/minus>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 P and homocysteine and was influenced by TNFRSFIB genotype. Thus genetic variation in or near the TNFRSFIB locus may predispose to CAD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 12:20:14