通过位于 1p13 胆固醇基因座的 SORT1 从非编码变异到表型。
From noncoding variant to phenotype via SORT1 at the 1p13 cholesterol locus.
机构信息
Cardiovascular Research Center and Center for Human Genetic Research, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
出版信息
Nature. 2010 Aug 5;466(7307):714-9. doi: 10.1038/nature09266.
Recent genome-wide association studies (GWASs) have identified a locus on chromosome 1p13 strongly associated with both plasma low-density lipoprotein cholesterol (LDL-C) and myocardial infarction (MI) in humans. Here we show through a series of studies in human cohorts and human-derived hepatocytes that a common noncoding polymorphism at the 1p13 locus, rs12740374, creates a C/EBP (CCAAT/enhancer binding protein) transcription factor binding site and alters the hepatic expression of the SORT1 gene. With small interfering RNA (siRNA) knockdown and viral overexpression in mouse liver, we demonstrate that Sort1 alters plasma LDL-C and very low-density lipoprotein (VLDL) particle levels by modulating hepatic VLDL secretion. Thus, we provide functional evidence for a novel regulatory pathway for lipoprotein metabolism and suggest that modulation of this pathway may alter risk for MI in humans. We also demonstrate that common noncoding DNA variants identified by GWASs can directly contribute to clinical phenotypes.
最近的全基因组关联研究(GWAS)已经确定了位于 1 号染色体 1p13 上的一个基因座,该基因座与人类血浆低密度脂蛋白胆固醇(LDL-C)和心肌梗死(MI)均有强烈关联。在这里,我们通过在人类队列和人源性肝细胞中的一系列研究表明,1p13 基因座上的一个常见非编码多态性 rs12740374 可创建 C/EBP(CCAAT/增强子结合蛋白)转录因子结合位点,并改变 SORT1 基因的肝表达。通过在小鼠肝脏中使用小干扰 RNA(siRNA)敲低和病毒过表达,我们证明 Sort1 通过调节肝 VLDL 分泌来改变血浆 LDL-C 和极低密度脂蛋白(VLDL)颗粒水平。因此,我们为脂蛋白代谢的新调节途径提供了功能证据,并表明该途径的调节可能会改变人类患 MI 的风险。我们还证明,GWAS 确定的常见非编码 DNA 变体可直接导致临床表型。
相似文献
N Engl J Med. 2010-12-16
J Lipid Res. 2023-12
Rev Port Cardiol. 2013-10
Nature. 2010-8-5
J Clin Invest. 2012-4-2
引用本文的文献
本文引用的文献
Arterioscler Thromb Vasc Biol. 2009-9-3
Obesity (Silver Spring). 2009-9