CD14 C260T promoter polymorphism and the risk of cerebrovascular diseases: a meta-analysis

• Autorzy: Banerjee I
• Języki publikacji: EN

Abstrakty

EN

Cerebrovascular diseases (CVD) are dysfunctions of the brain, resulting from diseases of blood vessels supplying the brain. Atherosclerosis is one of the major underlying causes of CVD, in which inflammation plays a crucial role. One of the inflammatory mechanisms contributing to atherogenesis is the activation of monocytes and macrophages, which could be mediated by the bacterial endotoxin lipopolysaccharide (LPS) via its receptor CD 14. The C260T (rs2569190) single-nucleotide polymorphism (SNP) in the promoter region of the CD 14 gene was implicated in CVD. To assess the role of this SNP in CVD, a comprehensive meta-analysis of the available genetic data was conducted. All the case-control association studies evaluating the role of CD14 C260T in CVD were identified. Of these, 7 studies (comprising a total of 1488 patients and 1600 control subjects) were included in this meta-analysis. To measure the strength of genetic association for the gene variant, the odds ratios (ORs) were calculated using both fixed and random effects for comparisons of the alleles, the genotypes, and the dominant and recessive genotype models. The results showed there was no significant association between the T allele of C260T and the risk of CVD under the fixed effects model, OR = 0.99 (95% CI (0.89, 1.09)), P = 0.84; or the random effects model, OR = 0.99 (95% CI (0.88, 1.11)), P = 0.83. Similar results were obtained for the homozygotes and the dominant and recessive models. In conclusion, the results of this meta-analysis suggest the CD14 C260T polymorphism is not a risk factor for CVD. However, more studies in ethnically varied populations are needed to evaluate in a reliable manner the role of this SNP in CVD susceptibility.

• Wydawca: -
• Czasopismo: Journal of Applied Genetics
• Rocznik: 2009
• Tom: 50
• Numer: 2
• Opis fizyczny: p.153-157,fig.,ref.

Twórcy

autor

Banerjee I

• Institute of Biochemistry, Swiss Federal Institute of Technology [ETH], Institute of Biochemistry, HPM E10.1, Schafmattstrasse 18, CH-8093, Zurich, Switzerland

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