Linked Life Data

12136229

Source:http://linkedlifedata.com/resource/pubmed/id/12136229

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-7-23
pubmed:abstractText
Heme oxygenase is a rate-limiting enzyme in heme degradation, leading to the generation of free iron, biliverdin, and carbon monoxide. Induction of heme oxygenase-1 is implicated in the antioxidant defense mechanism and can modulate vascular function. To test the association of microsatellite polymorphism in the promoter region of human HO-1 gene with the risk of coronary artery disease (CAD) in type 2 diabetic patients, we examined the allele frequencies of (GT) (n) repeats in HO-1 gene in 474 patients with CAD and in 322 controls. A transient-transfection assay with HO-1 promoter/luciferase fusion constructs carrying various lengths of (GT) (n) repeats was performed to explore the regulatory effect of (GT) (n) repeats on HO-1 gene expression in cultured rat aortic smooth muscle cells. Serum thiobarbituric acid-reactive substances (TBARs), a measure of lipid peroxidation, was significantly higher in subjects carrying the L/L genotype (> or =32 repeats). Among type 2 diabetic subjects, the frequencies of the L alleles and proportion of genotypes with L alleles were significantly higher in those with CAD than in those without CAD. The adjusted odds ratio for CAD in type 2 diabetic patients with L alleles was 4.7 (95% confidence interval, 1.9-12.0, P=0.001). Transfection experiments in aortic smooth muscle cells revealed that HO-1 promoter/luciferase fusion constructs containing longer (GT) (n) repeats exhibited lower transcriptional activity. These results imply that the length polymorphism in the HO-1 gene promoter modulate the transcription of the gene in vascular cells. Type 2 diabetics carrying longer (GT) (n) repeats might have higher oxidative stress and increased susceptibility to the development of CAD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0340-6717
pubmed:author
pubmed:issnType
Print
pubmed:volume
111
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:12136229-Aged, pubmed-meshheading:12136229-Animals, pubmed-meshheading:12136229-Coronary Artery Disease, pubmed-meshheading:12136229-Diabetes Mellitus, Type 2, pubmed-meshheading:12136229-Female, pubmed-meshheading:12136229-Genetic Predisposition to Disease, pubmed-meshheading:12136229-Heme Oxygenase (Decyclizing), pubmed-meshheading:12136229-Heme Oxygenase-1, pubmed-meshheading:12136229-Humans, pubmed-meshheading:12136229-Luciferases, pubmed-meshheading:12136229-Male, pubmed-meshheading:12136229-Membrane Proteins, pubmed-meshheading:12136229-Microsatellite Repeats, pubmed-meshheading:12136229-Muscle, Smooth, Vascular, pubmed-meshheading:12136229-Polymerase Chain Reaction, pubmed-meshheading:12136229-Polymorphism, Genetic, pubmed-meshheading:12136229-Promoter Regions, Genetic, pubmed-meshheading:12136229-Rats, pubmed-meshheading:12136229-Thiobarbituric Acid Reactive Substances, pubmed-meshheading:12136229-Transfection
pubmed:year
2002
pubmed:articleTitle
Microsatellite polymorphism in promoter of heme oxygenase-1 gene is associated with susceptibility to coronary artery disease in type 2 diabetic patients.
pubmed:affiliation
Institute of Clinical Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan, Republic of China.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't