title: Influence of eotaxin 67G>A polymorphism on plasma eotaxin concentrations in myocardial infarction survivors and healthy controls.
abstract: Eotaxin (CCL11) is a CC chemokine, whose systemic levels might be associated with coronary artery disease (CAD) and genetic variants predispose to the myocardial infarction (MI). However, the relationship between eotaxin genetic variants and plasma concentrations in CAD patients is still incompletely characterized. We genotyped 311 patients, who survived first MI and 338 controls for a 67G>A single nucleotide polymorphism in the eotaxin gene. By measuring plasma eotaxin concentrations in those subjects we related the former to the presence of 67G>A SNP. There were no differences in eotaxin genotype frequencies between patients and controls. Patient G/G carriers had higher circulating eotaxin levels compared both to G/A and A/A patients (P=0.046) and G/G controls (P=0.028), which might indicate the influence of additional factors (e.g. inflammatory mediators) on eotaxin secretion in those patients. At the same time, eotaxin levels did not differ between patients and controls irrespective of the 67G>A SNP variants they carried. There were no associations between plasma eotaxin levels, biochemical indicators of CAD and the degree of coronary artery stenosis in post-MI patients. Interestingly, some medications taken by the patients (e.g. diuretics and short-acting nitrates) might affect plasma eotaxin levels. In conclusion, our results show that there is no clear association between the presence of eotaxin 67G>A SNP, its plasma levels and CAD parameters in post-MI patients and that circulating eotaxin levels do not differ between subjects with clinical manifestations of coronary atherosclerosis and healthy controls.
authors.affiliation: Experimental Cardiovascular Research Unit, Center for Molecular Medicine L8:03, Karolinska University Hospital, SE-17176, Stockholm, Sweden. yuri.sheikine@cmm.ki.se
authors.forename: Yuri
authors.initials: Y
authors.lastname: Sheikine
authors.forename: Birgitta
authors.initials: B
authors.lastname: Olsen
authors.forename: Baback
authors.initials: B
authors.lastname: Gharizadeh
authors.forename: Ken
authors.initials: K
authors.lastname: Jatta
authors.forename: Per
authors.initials: P
authors.lastname: Tornvall
authors.forename: Mehran
authors.initials: M
authors.lastname: Ghaderi
mesh_terms: D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000097:blood* / Q000235:genetics*; D002631:Chemotactic Factors, Eosinophil; D004247:DNA / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D005787:Gene Frequency; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000235:genetics / Q000401:mortality; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D012189:Retrospective Studies; D012720:Severity of Illness Index; D015996:Survival Rate; D013548:Sweden / Q000453:epidemiology
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D004247:DNA