Zhao Bijun, Lin Yuan, Xu Jing, Ni Bixian, Da Min, Ding Chenyue, Hu Yuanli, Zhang Kai, Yang Shiwei, Wang Xiaowei, Yu Shiqiang, Chen Yijiang, Mo Xuming, Liu Jiayin, Shen Hongbing, Sha Jiahao, Ma Hongxia
Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China; Department of Epidemiology and Biostatistics and Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China.
PLoS One. 2014 Sep 12;9(9):e107411. doi: 10.1371/journal.pone.0107411. eCollection 2014.
Congenital heart disease (CHD) is the most common form of congenital human birth anomalies and a leading cause of perinatal and infant mortality. Some studies including our published genome-wide association study (GWAS) of CHD have indicated that genetic variants may contribute to the risk of CHD. Recently, Cordell et al. published a GWAS of multiple CHD phenotypes in European Caucasians and identified 3 susceptibility loci (rs870142, rs16835979 and rs6824295) for ostium secundum atrial septal defect (ASD) at chromosome 4p16. However, whether these loci at 4p16 confer the predisposition to CHD in Chinese population is unclear. In the current study, we first analyzed the associations between these 3 single nucleotide polymorphisms (SNPs) at 4p16 and CHD risk by using our existing genome-wide scan data and found all of the 3 SNPs showed significant associations with ASD in the same direction as that observed in Cordell's study, but not with other subtypes- ventricular septal defect (VSD) and ASD combined VSD. As these 3 SNPs were in high linkage disequilibrium (LD) in Chinese population, we selected one SNP with the lowest P value in our GWAS scan (rs16835979) to perform a replication study with additional 1,709 CHD cases with multiple phenotypes and 1,962 controls. The significant association was also observed only within the ASD subgroup, which was heterogeneous from other disease groups. In combined GWAS and replication samples, the minor allele of rs16835979 remained significant association with the risk of ASD (OR = 1.22, 95% CI = 1.08-1.38, P = 0.001). Our findings suggest that susceptibility loci of ASD identified from Cordell's European GWAS are generalizable to Chinese population, and such investigation may provide new insights into the roles of genetic variants in the etiology of different CHD phenotypes.
先天性心脏病(CHD)是人类先天性出生缺陷最常见的形式,也是围产期和婴儿死亡的主要原因。包括我们发表的先天性心脏病全基因组关联研究(GWAS)在内的一些研究表明,基因变异可能会增加患先天性心脏病的风险。最近,科德尔等人发表了一项针对欧洲白种人多种先天性心脏病表型的全基因组关联研究,并在染色体4p16上确定了3个继发孔型房间隔缺损(ASD)的易感位点(rs870142、rs16835979和rs6824295)。然而,4p16上的这些位点是否会使中国人群易患先天性心脏病尚不清楚。在本研究中,我们首先利用现有的全基因组扫描数据分析了4p16上这3个单核苷酸多态性(SNP)与先天性心脏病风险之间的关联,发现这3个SNP与房间隔缺损的关联均与科德尔研究中观察到的方向一致,但与其他亚型——室间隔缺损(VSD)以及房间隔缺损合并室间隔缺损无关。由于这3个SNP在中国人群中处于高度连锁不平衡(LD)状态,我们在全基因组关联研究扫描中选择了P值最低的一个SNP(rs16835979),对另外1709例具有多种表型的先天性心脏病病例和1962例对照进行复制研究。同样仅在房间隔缺损亚组中观察到显著关联,该亚组与其他疾病组不同。在全基因组关联研究和复制样本的合并分析中,rs16835979的次要等位基因与房间隔缺损风险仍存在显著关联(OR = 1.22,95%CI = 1.08 - 1.38,P = 0.001)。我们的研究结果表明,从科德尔的欧洲全基因组关联研究中确定的房间隔缺损易感位点在中国人中具有普遍性,此类研究可能为基因变异在不同先天性心脏病表型病因学中的作用提供新的见解。