Association between three single nucleotide polymorphisms in eotaxin (CCL 11) gene, hexanucleotide repetition upstream, severity and course of coronary atherosclerosis
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Blood Vessels pathology MeSH
- Chemokine CCL11 genetics MeSH
- Gene Frequency genetics MeSH
- Genetic Predisposition to Disease MeSH
- Genetic Association Studies * MeSH
- Polymorphism, Single Nucleotide genetics MeSH
- Middle Aged MeSH
- Humans MeSH
- Molecular Sequence Data MeSH
- Coronary Artery Disease genetics pathology MeSH
- Nucleotides genetics MeSH
- Disease Progression MeSH
- Repetitive Sequences, Nucleic Acid genetics MeSH
- Base Sequence MeSH
- Aged MeSH
- Case-Control Studies MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- CCL11 protein, human MeSH Browser
- Chemokine CCL11 MeSH
- Nucleotides MeSH
The impact of three single-nucleotide polymorphisms in eotaxin (SCYA11) gene promoter (-426C>T and -384A>G) and first exon (67G>A) and recently described hexanucleotide (GAAGGA)(n) 10.9 kb upstream on coronary atherosclerosis was investigated. Elective coronary angiography of 1050 consecutive subjects was performed. All patients were genotyped for the three SNPs. In a subset of the first 472 samples, the number of (GAAGGA)(n) repetitions was determined. For further evaluation, short and long variants were distinguished; the borderline corresponded with the median value of all alleles: ≤8 repetitions were considered as short sequence, ≥9 repetitions as long. Patients with bronchial asthma or insignificant atherosclerosis were excluded; the remaining group of 933 subjects was further investigated. Patients were grouped according to the form of CAD (ACS vs. stable angina) and the number of diseased vessels. The GG variant of 67 G>A polymorphism was associated with acute form of CAD compared to stable angina (p=0.0011, p(corr.)=0.013). The number of (GAAGGA)(n) repetitions in our set of patients ranged from 3 to 12. There were no subjects with 4 or 5 repetitions. The frequency of short repetition alleles increased with the number of affected vessels (1 vs. 3 diseased vessels: p=0.0043, p(corr)=0.034). In our study, the (GAAGGA)(n) hexanucleotide was associated with the severity of CAD. The 67 GG was associated with acute form of CAD. None of the two SNPs in eotaxin promoter had any relation to CAD. The number of (GAAGGA)(n) repetitions can thus be a novel genetic marker of the extent of CAD.
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Hum Genet. 2005 Nov;118(2):287-94 PubMed
Curr Cardiol Rep. 2010 Jul;12(4):338-43 PubMed
Biochem Biophys Res Commun. 1993 Dec 30;197(3):1167-72 PubMed
Stat Appl Genet Mol Biol. 2009;8:Article32 PubMed
J Allergy Clin Immunol. 2006 Feb;117(2):298-305 PubMed
Science. 1997 Sep 26;277(5334):2005-7 PubMed
Circulation. 2004 Aug 24;110(8):928-33 PubMed
J Immunol. 2002 Sep 1;169(5):2712-8 PubMed
J Clin Invest. 1996 Feb 1;97(3):604-12 PubMed
Atherosclerosis. 2006 Dec;189(2):458-63 PubMed
Physiol Rev. 2006 Apr;86(2):515-81 PubMed
Circulation. 2000 Oct 31;102(18):2185-9 PubMed
Circ Res. 1995 Sep;77(3):445-65 PubMed
Eur Heart J. 2010 Jun;31(12):1457-69 PubMed
J Med Genet. 2007 Jun;44(6):397-403 PubMed
Biochemistry. 1994 May 17;33(19):5674-81 PubMed
Cytokine. 2012 Feb;57(2):251-7 PubMed
Pathol Biol (Paris). 2006 Sep;54(7):375-86 PubMed
Clin Exp Dermatol. 2008 May;33(3):316-21 PubMed
Arterioscler Thromb Vasc Biol. 2011 May;31(5):969-79 PubMed
Atherosclerosis. 2006 May;186(1):140-5 PubMed
Physiol Genomics. 2007 Nov 14;31(3):402-9 PubMed
Int J Cardiol. 2001 Aug;80(1):55-60 PubMed
Br Heart J. 1993 Jan;69(1 Suppl):S38-41 PubMed
Arterioscler Thromb Vasc Biol. 2003 Sep 1;23(9):1510-20 PubMed
J Investig Med. 2006 Dec;54(8):446-54 PubMed
Lab Invest. 1988 Mar;58(3):249-61 PubMed
Arterioscler Thromb Vasc Biol. 2004 Jul;24(7):1211-6 PubMed
Proc Natl Acad Sci U S A. 1959 Jul;45(7):984-9 PubMed
Neurology. 2011 Sep 20;77(12):1165-73 PubMed
Genomics. 1997 May 1;41(3):471-6 PubMed
Atherosclerosis. 2005 Dec;183(2):268-74 PubMed
Pharmacol Ther. 2011 Sep;131(3):255-68 PubMed
Biochem Biophys Res Commun. 1997 Feb 13;231(2):365-8 PubMed
EMBO J. 1992 Oct;11(10):3777-86 PubMed
Atherosclerosis. 2004 Jul;175(1):91-4 PubMed
Genes Immun. 2001 Dec;2(8):461-3 PubMed
Ann N Y Acad Sci. 1985;454:115-20 PubMed
J Immunol. 2005 Feb 1;174(3):1525-31 PubMed