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首页> 外文期刊>BMC Medical Genomics >A genome-wide search replicates evidence of a quantitative trait locus for circulating angiotensin I-converting enzyme (ACE) unlinked to the ACE gene
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A genome-wide search replicates evidence of a quantitative trait locus for circulating angiotensin I-converting enzyme (ACE) unlinked to the ACE gene

机译：全基因组搜索可复制循环性血管紧张素I转换酶（ACE）与ACE基因不相关的定量性状基因座的证据

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Background Angiotensin I-converting enzyme (ACE) plays an important role in cardiovascular homeostasis. There is evidence from different ethnic groups that circulating ACE levels are influenced by a quantitative trait locus (QTL) at the ACE gene on chromosome 17. The finding of significant residual familial correlations in different ethnic groups, after accounting for this QTL, and the finding of support for linkage to a locus on chromosome 4 in Mexican-American families strongly suggest that there may well be QTLs for ACE unlinked to the ACE gene. Methods A genome-wide panel of microsatellite markers, and a panel of biallelic polymorphisms in the ACE gene were typed in Nigerian families. Single locus models with fixed parameters were used to test for linkage to circulating ACE with and without adjustment for the effects of the ACE gene polymorphisms. Results Strong evidence was found for D17S2193 (Zmax = 3.5); other nearby markers on chromosome 17 also showed modest support. After adjustment for the effects of the ACE gene locus, evidence of "suggestive linkage" to circulating ACE was found for D4S1629 (Zmax = 2.2); this marker is very close to a locus previously shown to be linked to circulating ACE levels in Mexican-American families. Conclusion In this report we have provided further support for the notion that there are QTLs for ACE unlinked to the ACE gene; our findings for chromosome 4, which appear to replicate the findings of a previous independent study, should be considered strong grounds for a more detailed examination of this region in the search for genes/variants which influence ACE levels. The poor yields, thus far, in defining the genetic determinants of hypertension risk suggest a need to look beyond simple relationships between genotypes and the ultimate phenotype. In addition to incorporating information on important environmental exposures, a better understanding of the factors which influence the building blocks of the blood pressure homeostatic network is also required. Detailed studies of the genetic determinants of ACE, an important component of the renin-angiotensin system, have the potential to contribute to this strategic objective.
机译：背景技术血管紧张素I转换酶（ACE）在心血管稳态中起重要作用。来自不同种族的证据表明，循环中的ACE水平受第17号染色​​体ACE基因上的数量性状基因座（QTL）的影响。在考虑了该QTL之后，发现了不同种族中显着的残留家族相关性，并且发现了关于墨西哥裔美国人家庭与4号染色体位点连锁的支持的强有力证据表明，很可能存在与ACE基因不连锁的ACE QTL。方法在尼日利亚家庭中，对全基因组微卫星标志物和ACE基因中的双等位基因多态性进行分型。具有固定参数的单基因座模型用于测试与循环ACE的连锁关系，无论是否调整ACE基因多态性的影响。结果找到了D17S2193的有力证据（Z max = 3.5）; 17号染色​​体上其他附近的标记也显示出适度的支持。调整ACE基因位点的作用后，发现D4S1629与循环ACE有“暗示性联系”（Z max = 2.2）。该标记非常接近先前显示与墨西哥裔美国人家庭中循环ACE水平相关的基因座。结论在本报告中，我们进一步支持以下观点：存在与ACE基因不相关的ACE QTL。我们对第4号染色体的发现似乎可以重复先前的独立研究的发现，应被视为更牢固地检查该区域以寻找影响ACE水平的基因/变体的有力依据。迄今为止，在确定高血压风险的遗传决定因素方面，单产低下表明需要超越基因型和最终表型之间的简单关系。除了纳入有关重要环境暴露的信息外，还需要更好地了解影响血压稳态网络组成部分的因素。 ACE（肾素-血管紧张素系统的重要组成部分）的遗传决定因素的详细研究可能有助于实现这一战略目标。

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