Journal of clinical laboratory analysis · 2022
Increased long non-coding RNA NORAD reflects serious cardiovascular stenosis, aggravated inflammation status, and higher lipid level in coronary heart disease.
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Zhang Xiaoyun, Kan Xuetong, Shen Jingjing, Li Jian
Аннотация
OBJECTIVE: Long non-coding RNA activated by DNA damage (lnc-NORAD) modulates inflammation, lipid level, and atherosclerosis in various cardiovascular diseases. This study intended to investigate the dysregulated expression of lnc-NORAD, and its linkage with clinical characteristics, inflammatory cytokines, and accumulating major adverse cardiovascular events (MACE) in coronary heart disease (CHD) patients.
METHODS: Totally, 160 CHD patients, 30 disease controls (DCs), and 30 healthy controls (HCs) were included. The reverse transcription-quantitative polymerase chain reaction was used to detect lnc-NORAD expression in peripheral blood mononuclear cell samples from all participants. Enzyme-linked immunosorbent assay was applied to detect proinflammatory cytokines and adhesion molecules in CHD patients. Then, MACE was recorded during a median follow-up of 12 (range: 1.0-27.0) months.
RESULTS: Lnc-NORAD was highest in CHD patients, followed by DCs, and lowest in HCs (p < 0.001). In CHD patients, lnc-NORAD was positively linked with Gensini score (p = 0.001). Meanwhile, lnc-NORAD was positively linked to C-reactive protein (p = 0.023), tumor necrosis factor-alpha (p = 0.016), interleukin (IL)-6 (p = 0.003), IL-8 (P = 0.018), and IL-17A (p = 0.029). No relation of lnc-NORAD with vascular cell adhesion molecule-1 (p = 0.094) and intercellular adhesion molecule-1 (p = 0.060) was found. Furthermore, lnc-NORAD was positively related to total cholesterol (p = 0.014) and low-density lipoprotein cholesterol (p = 0.004), whereas lnc-NORAD was not linked to triglyceride (p = 0.103) and high-density lipoprotein cholesterol (p = 0.533). However, lnc-NORAD (high vs. low), and its higher quartiles were both not linked to accumulating MACE rate (p > 0.05).
CONCLUSION: Increased lnc-NORAD is linked with aggravated stenosis degree, inflammation status, and blood lipid in CHD patients. However, further validation is required.
METHODS: Totally, 160 CHD patients, 30 disease controls (DCs), and 30 healthy controls (HCs) were included. The reverse transcription-quantitative polymerase chain reaction was used to detect lnc-NORAD expression in peripheral blood mononuclear cell samples from all participants. Enzyme-linked immunosorbent assay was applied to detect proinflammatory cytokines and adhesion molecules in CHD patients. Then, MACE was recorded during a median follow-up of 12 (range: 1.0-27.0) months.
RESULTS: Lnc-NORAD was highest in CHD patients, followed by DCs, and lowest in HCs (p < 0.001). In CHD patients, lnc-NORAD was positively linked with Gensini score (p = 0.001). Meanwhile, lnc-NORAD was positively linked to C-reactive protein (p = 0.023), tumor necrosis factor-alpha (p = 0.016), interleukin (IL)-6 (p = 0.003), IL-8 (P = 0.018), and IL-17A (p = 0.029). No relation of lnc-NORAD with vascular cell adhesion molecule-1 (p = 0.094) and intercellular adhesion molecule-1 (p = 0.060) was found. Furthermore, lnc-NORAD was positively related to total cholesterol (p = 0.014) and low-density lipoprotein cholesterol (p = 0.004), whereas lnc-NORAD was not linked to triglyceride (p = 0.103) and high-density lipoprotein cholesterol (p = 0.533). However, lnc-NORAD (high vs. low), and its higher quartiles were both not linked to accumulating MACE rate (p > 0.05).
CONCLUSION: Increased lnc-NORAD is linked with aggravated stenosis degree, inflammation status, and blood lipid in CHD patients. However, further validation is required.