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黄淑娜, 林佳冰, 黄清, 曾昭楠, 张周泽玥, 李煌元, 吴思英, 林少炜. 长链非编码RNAs(NR_027032、NR_047116及NR_104181)在冠心病发病中作用[J]. 中国公共卫生, 2020, 36(6): 909-912. DOI: 10.11847/zgggws1119452
引用本文: 黄淑娜, 林佳冰, 黄清, 曾昭楠, 张周泽玥, 李煌元, 吴思英, 林少炜. 长链非编码RNAs(NR_027032、NR_047116及NR_104181)在冠心病发病中作用[J]. 中国公共卫生, 2020, 36(6): 909-912. DOI: 10.11847/zgggws1119452
Shu-na HUANG, Jia-bing LIN, Qing HUANG, . Role of long-chain noncoding RNAs (NR_027032, NR_047116 and NR_104181) in pathogenesis of coronary atherosclerotic heart disease[J]. Chinese Journal of Public Health, 2020, 36(6): 909-912. DOI: 10.11847/zgggws1119452
Citation: Shu-na HUANG, Jia-bing LIN, Qing HUANG, . Role of long-chain noncoding RNAs (NR_027032, NR_047116 and NR_104181) in pathogenesis of coronary atherosclerotic heart disease[J]. Chinese Journal of Public Health, 2020, 36(6): 909-912. DOI: 10.11847/zgggws1119452

长链非编码RNAs(NR_027032、NR_047116及NR_104181)在冠心病发病中作用

Role of long-chain noncoding RNAs (NR_027032, NR_047116 and NR_104181) in pathogenesis of coronary atherosclerotic heart disease

  • 摘要:
      目的  检测并分析长链非编码RNAs(lncRNAs)在冠心病患者及氧化低密度脂蛋白(oxLDL)致人冠状动脉内皮细胞(HCAECs)损伤模型中的表达情况,为冠心病的表观遗传机制提供理论依据。
      方法  于2016年8月在福建医科大学附属第一医院和协和医院选择5个年龄相近、病情相当、病程相似且未合并其他疾病的冠心病病例和5个与病例组患者年龄、性别、文化程度、冠心病家族史、吸烟、饮酒、体质指数等无差异的非冠心病患者进行基因芯片表达谱检测,根据表达差异倍数结合生物学信息初步筛选与冠心病发病潜在相关的3条lncRNAs(NR_027032、NR_047116和NR_104181)在体外细胞中进行验证,并应用oxLDL诱导HCAECs损伤模型,分析以上3条lncRNAs的表达情况。
      结果  与对照组比较,50、100和150 µg/mL oxLDL处理组24、48和72 h的细胞活力均低于对照组(均P < 0.05),其中150 µg/mL oxLDL处理组的细胞活力最低,分别为(0.77 ± 0.14)、(0.53 ± 0.02)和(0.55 ± 0.01);在oxLDL干预致HCAECs损伤模型中,NR_027032、NR_047116和NR_104181表达水平均较对照组高,差异均有统计学意义(均P < 0.05)。
      结论  NR_027032、NR_047116和NR_104181在冠心病患者及oxLDL诱导的HCAECs损伤中表达异常,可能参与了冠心病的发生发展。

     

    Abstract:
      Objective  To detect and analyze the expression of long-chain noncoding RNAs (lncRNAs) in patients with coronary atherosclerotic heart disease (CAD) and oxidized low-density lipoprotein (oxLDL)-induced human coronary artery endothelial cells (HCAECs) injury model for providing a theoretical basis to researches on epigenetic mechanism of CAD.
      Methods  We enrolled 5 CAD patients (cases) with similar age, disease condition and duration and without other diseases, and 5 non-CAD patients (controls) matched for age, sex, education, family history of CAD, tobacco smoking, alcohol drinking and body mass index to the cases in the First Affiliated Hospital of Fujian Medical University and the Union Hospital of Fujian Medical University in August 2016. Peripheral blood samples of the participants were collected for detection of gene chip expression profile. Based on gene expression difference between the cases and the controls and previous biological information studies, we screened out 3 lncRNAs (NR_027032, NR_047116, and NR_104181) potentially related to the pathogenesis of CAD for validation in vitro. The oxLDL-induced HCAECs injury model was used to analyze expressions of the 3 lncRNAs selected.
      Results  The viabilities of HCAECs treated with 50, 100 and 150 µg/mL oxLDL were all lower than those of the control cells at 24, 48 and 72 hours (all P < 0.05), and the viabilities of the HCAECs treated with 150 µg/mL oxLDL were the lowest (0.77 ± 0.14, 0.53 ± 0.02, and 0.55 ± 0.01). The expressions of NR_027032, NR_047116, and NR_104181 in oxLDL-treated HCAECs were all significantly higher than those in the control cells (all P < 0.05).
      Conclusion  NR_027032, NR_047116 and NR_104181 are abnormally expressed in patients with CAD and oxLDL-induced injury HCAECs, and may be involved in the pathogenesis of CAD.

     

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