Reiner A P, Carty C L, Carlson C S, Wan J Y, Rieder M J, Smith J D, Rice K, Fornage M, Jaquish C E, Williams O D, Tracy R P, Lewis C E, Siscovick D S, Boerwinkle E, Nickerson D A
Departments of Epidemiology and Genome Sciences, University of Washington, Seattle, WA 98101-1448, USA.
J Thromb Haemost. 2006 Jun;4(6):1279-87. doi: 10.1111/j.1538-7836.2006.01907.x.
Previous genotype-phenotype association studies of fibrinogen have been limited by incomplete knowledge of genomic sequence variation within and between major ethnic groups in FGB, FGA, and FGG.
We characterized the linkage disequilibrium patterns and haplotype structure across the human fibrinogen gene locus in European- and African-American populations. We analyzed the association between common polymorphisms in the fibrinogen genes and circulating levels of both 'functional' fibrinogen (measured by the Clauss clotting rate method) and total fibrinogen (measured by immunonephelometry) in a large, multi-center, bi-racial cohort of young US adults.
A common haplotype tagged by the A minor allele of the well-studied FGB-455 G/A promoter polymorphism (FGB 1437) was confirmed to be strongly associated with increased plasma fibrinogen levels. Two non-coding variants specific to African-American chromosomes, FGA 3845 A and FGG 5729 G, were each associated with lower plasma fibrinogen levels. In European-Americans, a common haplotype tagged by FGA Thr312Ala and several other variant alleles across the fibrinogen gene locus was strongly associated with decreased fibrinogen levels as measured by functional assay, but not by immunoassay. Overall, common polymorphisms within the three fibrinogen genes explain < 2% of the variability in plasma fibrinogen concentration.
In young adults, fibrinogen multi-locus genotypes are associated with plasma fibrinogen levels. The specific single nucleotide polymorphism and haplotype patterns for these associations differ according to population and also according to phenotypic assay. It is likely that a substantial proportion of the heritable component of plasma fibrinogen concentration is due to genetic variation outside the three fibrinogen genes.
以往关于纤维蛋白原的基因型-表型关联研究受到对FGB、FGA和FGG主要种族群体内部及之间基因组序列变异了解不全面的限制。
我们对欧洲裔和非裔美国人群体中人类纤维蛋白原基因座的连锁不平衡模式和单倍型结构进行了特征分析。我们在一个大型、多中心、双种族的美国年轻成年人队列中,分析了纤维蛋白原基因常见多态性与“功能性”纤维蛋白原(通过Clauss凝血率法测量)和总纤维蛋白原(通过免疫比浊法测量)循环水平之间的关联。
由研究充分的FGB - 455 G/A启动子多态性(FGB 1437)的A次要等位基因标记的常见单倍型被证实与血浆纤维蛋白原水平升高密切相关。两个非裔美国人染色体特有的非编码变体,FGA 3845 A和FGG 5729 G,各自与较低的血浆纤维蛋白原水平相关。在欧洲裔美国人中,由FGA Thr312Ala和纤维蛋白原基因座上的其他几个变体等位基因标记的常见单倍型与通过功能测定法测量的纤维蛋白原水平降低密切相关,但通过免疫测定法测量则不然。总体而言,三个纤维蛋白原基因内的常见多态性解释了血浆纤维蛋白原浓度变异的不到2%。
在年轻成年人中,纤维蛋白原多基因座基因型与血浆纤维蛋白原水平相关。这些关联的特定单核苷酸多态性和单倍型模式因人群以及表型测定方法而异。血浆纤维蛋白原浓度的可遗传成分很可能有很大一部分归因于三个纤维蛋白原基因之外的遗传变异。