The human rs1050286 polymorphism alters LOX‐1 expression through modifying miR‐24 binding

• Published in: Journal of cellular and molecular medicine Vol. 20; no. 1; pp. 181 - 187
• Main Authors: Morini, Elena, Rizzacasa, Barbara, Pucci, Sabina, Polidoro, Chiara, Ferrè, Fabrizio, Caporossi, Daniela, Helmer Citterich, Manuela, Novelli, Giuseppe, Amati, Francesca
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.01.2016; John Wiley and Sons Inc
• Subjects: 3' Untranslated Regions; acute myocardial infarction; Algorithms; alternative splicing; Apoptosis; Arteriosclerosis; Atherosclerosis; Base Sequence; Binding Sites; Cardiomyocytes; Cell lines; Coronary artery; Coronary Artery Disease - genetics; Enzyme Repression; Gene expression; Gene silencing; Genetic Association Studies; Genetic Predisposition to Disease; Haplotypes; Heart attacks; HeLa Cells; Hep G2 Cells; Hsa‐mir‐24; Humans; MicroRNAs; MicroRNAs - genetics; MicroRNAs - metabolism; Myocardial infarction; Myocardial Infarction - genetics; Nociceptin receptors; OLR1 gene; Polymorphism, Single Nucleotide; Receptor density; Ribonucleic acid; RNA; RNA Interference; Scavenger Receptors, Class E - genetics; Scavenger Receptors, Class E - metabolism; Sequence Analysis, RNA; Short Communication; Single-nucleotide polymorphism; Software; United States > US; alternative splicing; Hsa-mir-24; OLR1 gene; acute myocardial infarction; Atherosclerosis

The up‐regulation of lectin‐like oxidized low‐density lipoprotein receptor‐1 (LOX‐1), encoded by the OLR1 gene, plays a fundamental role in the pathogenesis of atherosclerosis. Moreover, OLR1 polymorphisms were associated with increased susceptibility to acute myocardial infarction (AMI) and coronar...