White Marquitta J, Kodaman Nuri M, Harder Reed H, Asselbergs Folkert W, Vaughan Douglas E, Brown Nancy J, Moore Jason H, Williams Scott M
Center for Human Genetics Research, Vanderbilt University, Nashville, Tennessee, United States of America; Department of Genetics and Institute of Quantitative Biomedical Sciences, Dartmouth College, Hanover, New Hampshire, United States of America.
Department of Genetics and Institute of Quantitative Biomedical Sciences, Dartmouth College, Hanover, New Hampshire, United States of America.
PLoS One. 2015 Aug 31;10(8):e0136379. doi: 10.1371/journal.pone.0136379. eCollection 2015.
Plasminogen activator inhibitor 1 (PAI-1), a major modulator of the fibrinolytic system, is an important factor in cardiovascular disease (CVD) susceptibility and severity. PAI-1 is highly heritable, but the few genes associated with it explain only a small portion of its variation. Studies of PAI-1 typically employ linear regression to estimate the effects of genetic variants on PAI-1 levels, but PAI-1 is not normally distributed, even after transformation. Therefore, alternative statistical methods may provide greater power to identify important genetic variants. Additionally, most genetic studies of PAI-1 have been performed on populations of European descent, limiting the generalizability of their results. We analyzed >30,000 variants for association with PAI-1 in a Ghanaian population, using median regression, a non-parametric alternative to linear regression. Three variants associated with median PAI-1, the most significant of which was in the gene arylsulfatase B (ARSB) (p = 1.09 x 10(-7)). We also analyzed the upper quartile of PAI-1, the most clinically relevant part of the distribution, and found 19 SNPs significantly associated in this quartile. Of note an association was found in period circadian clock 3 (PER3). Our results reveal novel associations with median and elevated PAI-1 in an understudied population. The lack of overlap between the two analyses indicates that the genetic effects on PAI-1 are not uniform across its distribution. They also provide evidence of the generalizability of the circadian pathway's effect on PAI-1, as a recent meta-analysis performed in Caucasian populations identified another circadian clock gene (ARNTL).
纤溶酶原激活物抑制剂1(PAI-1)是纤维蛋白溶解系统的主要调节因子,是心血管疾病(CVD)易感性和严重程度的重要因素。PAI-1具有高度遗传性,但与之相关的少数基因仅解释了其变异的一小部分。对PAI-1的研究通常采用线性回归来估计基因变异对PAI-1水平的影响,但即使经过转换,PAI-1也不呈正态分布。因此,替代统计方法可能会提供更大的效力来识别重要的基因变异。此外,大多数关于PAI-1的基因研究是在欧洲血统人群中进行的,限制了其结果的普遍性。我们在加纳人群中使用中位数回归(线性回归的非参数替代方法)分析了超过30000个与PAI-1相关的变异。三个变异与PAI-1中位数相关,其中最显著的一个位于芳基硫酸酯酶B(ARSB)基因中(p = 1.09 x 10^(-7))。我们还分析了PAI-1的上四分位数(分布中最具临床相关性的部分),并在此四分位数中发现了19个显著相关的单核苷酸多态性(SNP)。值得注意的是,在周期昼夜节律时钟3(PER3)中发现了一种关联。我们的结果揭示了在一个研究较少的人群中与PAI-1中位数和升高水平的新关联。两项分析之间缺乏重叠表明,对PAI-1的遗传效应在其分布中并不均匀。它们还提供了昼夜节律途径对PAI-1影响具有普遍性的证据,因为最近在白种人群中进行的一项荟萃分析确定了另一个昼夜节律时钟基因(ARNTL)。