Document Detail


The intron 6 G/T polymorphism of c-myb oncogene and the risk for coronary in-stent restenosis.
MedLine Citation:
PMID:  15221349     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The principle mechanisms leading to the development of atherosclerosis are long-term accumulation of lipids and cell proliferation. We have recently shown that a single nucleotide polymorphism in the c-myb gene is associated with the development of coronary artery disease in humans and intracellular lipid accumulation. C-myb expression has been further shown to be up-regulated during cell proliferation. The development of in-stent restenosis is predominantly driven by smooth muscle cell proliferation. METHODS: To study a possible association of c-myb with neointima formation in humans we genotyped 485 consecutive patients undergoing coronary stenting for a G/T-single nucleotide polymorphism in intron 6 of the cmyb gene. Restenosis was assessed by quantitative coronary angiography and angiographic follow-up after 6 months. To study the effect of c-myb on smooth muscle cell proliferation primary human smooth muscle cells were infected with recombinant adenovirus expressing c-myb, a dominant negative myb-engrailed fusion protein or control virus. RESULTS AND CONCLUSION: Restenosis > 50% occurred in 27.6% of patients with at least one G-allele and in 20.8% of those without (p = 0.10). Even after adjustment for the independent risk factors diabetes mellitus, reference lumen diameter, smoking, dyslipidemia and number of diseased vessels, the observed difference in the distribution of the c-myb alleles did not reach statistical significance (p = 0.08). Adenoviral gene transfer of c-myb did not increase proliferation of cultured smooth muscle compared to control virus or untransfected cells, while the expression of the dominant negative mutant reduced proliferation of VSMC as previously shown. Our results indicate that expression of c-myb, while being important for cell cycle is not sufficient to induce smooth muscle cell proliferation. The G/T-nucleotide transversion polymorphism in intron 6 of the c-myb oncogene that has been associated with atherosclerosis and lipid accumulation is not a risk factor for human in-stent restenosis.
Authors:
C Michael Gross; Jochen Krämer; Arne Pfeufer; Rainer Dietz; Reinhard Gessner; Michael Praus
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Publication Detail:
Type:  Journal Article     Date:  2004-04-16
Journal Detail:
Title:  Basic research in cardiology     Volume:  99     ISSN:  0300-8428     ISO Abbreviation:  Basic Res. Cardiol.     Publication Date:  2004 Jul 
Date Detail:
Created Date:  2004-06-28     Completed Date:  2005-02-08     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0360342     Medline TA:  Basic Res Cardiol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  309-14     Citation Subset:  IM    
Affiliation:
HELIOS-Clinic Berlin, Franz Volhard Clinic at Max Delbrück Center for Molecular Medicine, Medical Faculty of the Charité Humboldt University, Wiltberg Strasse 50, 13125 Berlin, Germany. gross@fvk-berlin.de
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MeSH Terms
Descriptor/Qualifier:
Coronary Angiography
Coronary Artery Bypass*
Coronary Artery Disease / genetics
Female
Follow-Up Studies
Genes, myc*
Genotype
Glycine
Graft Occlusion, Vascular / genetics*
Humans
Introns
Male
Polymorphism, Genetic*
Polymorphism, Single Nucleotide*
Risk Factors
Stents*
Threonine
Time Factors
Up-Regulation
Chemical
Reg. No./Substance:
56-40-6/Glycine; 72-19-5/Threonine
Comments/Corrections
Erratum In:
Basic Res Cardiol. 2004 Jul;99(4):315

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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