Ischemic stroke susceptibility gene in a Northern Han Chinese population

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Abstract

Research Highlights

(1) A serum amyloid A gene polymorphism is positively correlated with carotid intima-media thickness in the healthy Han Chinese population. However, the correlation between this serum amyloid A polymorphism and ischemic cerebrovascular disease is not yet known. Interleukin-18 is closely related to atherosclerotic plaque progression and instability. Interleukin-18 promoter gene polymorphisms may be associated with ischemic stroke pathogenesis, and the -607C allele increases ischemic stroke risk in the Han Chinese population. The frequency distribution of genetic polymorphisms varies among different populations, races, and living environments.

Research Highlights

(2) In the present study, we analyzed serum amyloid A and interleukin-18 levels in a Han Chinese population to investigate the relationship between serum amyloid A, interleukin-18, and C-reactive protein, as well as their role in ischemic cerebrovascular disease.

Research Highlights

(3) The -13T/C (rs11024595) polymorphism, in the 5′-flanking region of the serum amyloid A gene, shows no correlation with ischemic cerebrovascular disease. However, the C allele of the -607C/A (rs1946518) polymorphism in the interleukin-18 gene promoter is a strong risk factor for ischemic cerebrovascular disease in the Han population of northern China. In addition, the A allele is likely protective for ischemic cerebrovascular disease.

Interleukin-18 gene promoter polymorphisms are potential risk factors for ischemic cerebrovascular disease, and the -607C allele may increase ischemic stroke risk in the Han Chinese population. In the present study, we recruited 291 patients with ischemic cerebrovascular disease from the Affiliated Hospital of Qingdao University Medical College, China, and 226 healthy controls. Both patients and controls were from the Han population in northern China. Immunoresonance scattering assays detected increased serum amyloid A protein, C-reactive protein, and interleukin-18 levels in ischemic cerebrovascular disease patients compared with healthy controls. Analysis of the -607C/A (rs1946518) polymorphism in the interleukin-18 gene promoter showed ischemic cerebrovascular disease patients exhibited increased frequencies of the CC genotype and C alleles than healthy controls. Genotype and allele frequencies of the interleukin-18 -137G/C (rs187238) polymorphism and the -13T/C (rs11024595) polymorphism in the 5′-flanking region of serum amyloid A, showed no significant difference between the two groups. Multivariate logistic regression analysis on the interleukin-18 promoter A/C genetic locus, for correction of age, gender, history of smoking, hypertension, diabetes mellitus, hypercholesteremia, and an ischemic stroke family history, showed ischemic cerebrovascular disease risk in individuals without the A allele (C homozygotes) was 2.2-fold greater than in A allele carriers. Overall, our findings suggest that the -13T/C (rs11024595) polymorphism in the 5′-flanking region of serum amyloid A has no correlation with ischemic cerebrovascular disease, but the C allele of the -607C/A (rs1946518) polymorphism in the interleukin-18 promoter is a high-risk factor for ischemic cerebrovascular disease in the Han population of northern China. In addition, the A allele is likely a protective gene for ischemic cerebrovascular disease.

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