{"title":"中国汉族人群中LncRNA RP1-276N6.2的表达和RP1-276N8.2基因多态性与冠心病风险的关系。","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":"{\"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}","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
摘要
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
LncRNA RP1-276N6.2 Expression and RP1-276N6.2 Gene Polymorphisms Contribute to the Risk of Coronary Artery Disease in Chinese Han Population.
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.