{"title":"LncRNA RP1-276N6.2 Expression and RP1-276N6.2 Gene Polymorphisms Contribute to the Risk of Coronary Artery Disease in Chinese Han Population.","authors":"Lijuan Chen, Mingming Zhao, Mingsha Zhou, Jia Luo, Shan Li, Xing Liu, Zheng Cheng, Yang Zhuo, Weiqi Zeng, Zhiyu Zhang, Li Zhou","doi":"10.1089/dna.2023.0202","DOIUrl":null,"url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) have been implicated in coronary artery disease (CAD) processes. However, the relationship between the gene polymorphisms of lncRNA RP1-276N6.2 as a novel molecule and susceptibility to CAD remains unclear. In our case-control study, 949 CAD patients and 892 healthy controls were genotyped using the TaqMan genotyping assay. The quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay were performed to examine the expression levels of RP1-276N6.2 and SLC22A3(OCT3). We observed that CAD patients had significantly lower RP1-276N6.2 levels than those healthy participants (<i>p</i> < 0.05). Compared to the wild-type genotype, the rs611950 T allele and the rs10499313 AG genotype and G allele significantly increased the premature CAD risk (<i>p</i> = 0.02, <i>p</i> = 0.002, and <i>p</i> = 0.01, respectively), while the rs505000 G allele reduced this risk (<i>p</i> = 0.01); moreover, the rs505000 CG genotype significantly enhanced the delayed CAD risk (<i>p</i> = 0.03), and the rs505000 G allele reduced the expression levels of RP1-276N6.2 and SLC22A3 (<i>p</i> < 0.05 and <i>p</i> < 0.05, respectively). In addition, RP1-276N6.2 positively regulated the mRNA and secreted protein levels of SLC22A3 (<i>p</i> < 0.05). In conclusion, the RP1-276N6.2 gene polymorphisms were closely associated with CAD risk. LncRNA RP1-276N6.2 may be a potential genetic target for CAD early diagnosis and treatment.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"746-752"},"PeriodicalIF":0.0000,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"DNA and cell biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/dna.2023.0202","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/10/16 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Long noncoding RNAs (lncRNAs) have been implicated in coronary artery disease (CAD) processes. However, the relationship between the gene polymorphisms of lncRNA RP1-276N6.2 as a novel molecule and susceptibility to CAD remains unclear. In our case-control study, 949 CAD patients and 892 healthy controls were genotyped using the TaqMan genotyping assay. The quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay were performed to examine the expression levels of RP1-276N6.2 and SLC22A3(OCT3). We observed that CAD patients had significantly lower RP1-276N6.2 levels than those healthy participants (p < 0.05). Compared to the wild-type genotype, the rs611950 T allele and the rs10499313 AG genotype and G allele significantly increased the premature CAD risk (p = 0.02, p = 0.002, and p = 0.01, respectively), while the rs505000 G allele reduced this risk (p = 0.01); moreover, the rs505000 CG genotype significantly enhanced the delayed CAD risk (p = 0.03), and the rs505000 G allele reduced the expression levels of RP1-276N6.2 and SLC22A3 (p < 0.05 and p < 0.05, respectively). In addition, RP1-276N6.2 positively regulated the mRNA and secreted protein levels of SLC22A3 (p < 0.05). In conclusion, the RP1-276N6.2 gene polymorphisms were closely associated with CAD risk. LncRNA RP1-276N6.2 may be a potential genetic target for CAD early diagnosis and treatment.
长链非编码RNA(lncRNA)与冠状动脉疾病(CAD)过程有关。然而,lncRNA RP1-276N6.2作为一种新分子的基因多态性与CAD易感性之间的关系尚不清楚。在我们的病例对照研究中,使用TaqMan基因分型法对949名CAD患者和892名健康对照进行了基因分型。采用实时定量聚合酶链反应和酶联免疫吸附法检测RP1-276N6.2和SLC22A3(OCT3)的表达水平。我们观察到CAD患者的RP1-276N6.2水平显著低于健康参与者(p p = 0.02,p = 0.002和p = 分别为0.01),而rs505000G等位基因降低了这种风险(p = 0.01);此外,rs505000CG基因型显著增加了延迟性CAD的风险(p = 0.03),rs505000G等位基因降低了RP1-276N6.2和SLC22A3的表达水平(p p p