Wang Ermin, Zhao Hainan, Zhao Deyan, Li Lijing, Du Limin
Department of Nephrology, The First Affiliated Hospital, Jinzhou Medical University, Jinzhou, China.
Jinzhou Medical University, Jinzhou, China.
Front Genet. 2018 Dec 3;9:573. doi: 10.3389/fgene.2018.00573. eCollection 2018.
The genetic predisposition to chronic kidney disease (CKD) has been widely evaluated especially using the genome-wide association studies, which highlighted some novel genetic susceptibility variants in many genes, and estimated glomerular filtration rate to diagnose and stage CKD. Of these variants, rs7805747 in PRKAG2 was identified to be significantly associated with both serum creatinine and CKD with genome wide significance level. Until now, the potential mechanism by which rs7805747 affects CKD risk is still unclear. Here, we performed a functional analysis of rs7805747 variant using multiple bioinformatics software and databases. Using RegulomeDB and HaploReg (version 4.1), rs7805747 was predicated to locate in enhancer histone marks (Liver, Duodenum Mucosa, Fetal Intestine Large, Fetal Intestine Small, and Right Ventricle tissues). Using GWAS analysis in PhenoScanner, we showed that rs7805747 is not only associated with CKD, but also is significantly associated with other diseases or phenotypes. Using metabolite analysis in PhenoScanner, rs7805747 is identified to be significantly associated with not only the serum creatinine, but also with other 16 metabolites. Using eQTL analysis in PhenoScanner, rs7805747 is identified to be significantly associated with gene expression in multiple human tissues and multiple genes including PRKAG2. The gene expression analysis of PRKAG2 using 53 tissues from GTEx RNA-Seq of 8555 samples (570 donors) in GTEx showed that PRKAG2 had the highest median expression in Heart-Atrial Appendage. Using the gene expression profiles in human CKD, we further identified different expression of PRKAG2 gene in CKD cases compared with control samples. In summary, our findings provide new insight into the underlying susceptibility of PRKAG2 gene to CKD.
慢性肾脏病(CKD)的遗传易感性已得到广泛评估,尤其是通过全基因组关联研究,该研究突出了许多基因中的一些新的遗传易感性变异,并利用估计的肾小球滤过率来诊断CKD并进行分期。在这些变异中,PRKAG2基因中的rs7805747被确定与血清肌酐和CKD均显著相关,且具有全基因组显著性水平。到目前为止,rs7805747影响CKD风险的潜在机制仍不清楚。在此,我们使用多种生物信息学软件和数据库对rs7805747变异进行了功能分析。使用RegulomeDB和HaploReg(4.1版),预测rs7805747位于增强子组蛋白标记(肝脏、十二指肠黏膜、胎儿大肠、胎儿小肠和右心室组织)中。使用PhenoScanner中的GWAS分析,我们表明rs7805747不仅与CKD相关,还与其他疾病或表型显著相关。使用PhenoScanner中的代谢物分析,rs7805747不仅被确定与血清肌酐显著相关,还与其他16种代谢物相关。使用PhenoScanner中的eQTL分析,rs7805747被确定与多种人体组织和包括PRKAG2在内的多个基因的基因表达显著相关。使用来自GTEx中8555个样本(570个供体)的GTEx RNA-Seq的53个组织对PRKAG2进行基因表达分析,结果显示PRKAG2在心脏心耳中的中位表达最高。利用人类CKD中的基因表达谱,我们进一步确定了与对照样本相比,CKD病例中PRKAG2基因的不同表达。总之,我们的研究结果为PRKAG2基因对CKD的潜在易感性提供了新的见解。