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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

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

  •   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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