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The interplay of LncRNA ANRIL and miR-181b on the inflammation-relevant coronary artery disease through mediating NF-?B signalling pathway.

ABSTRACT: This study was designed to investigate whether ANRIL affected the aetiology of coronary artery disease (CAD) by acting on downstream miR-181b and NF-?B signalling. Altogether 327 CAD patients diagnosed by angiography were included, and mice models of CAD were established. Human coronary endothelial cells (HCAECs) and human umbilical vein endothelial cells (HUVECs) were also purchased. In addition, shRNA-ANRIL, shRNA-NC, pcDNA3.1-ANRIL, miR-181b mimic, miR-181b inhibitor and miR-NC were transfected into the cells. The lipopolysaccharides (LPS) and pyrrolidine dithiocarbamate (PDTC) were also added to activate or deactivate NF-?B signalling. Both highly expressed ANRIL and lowly expressed miR-181b were associated with CAD population aged over 60 years old, with smoking history, with hypertension and hyperlipidemia, with CHOL H 4.34 mmol/L, TG ? 1.93 mmol/L and Hcy ? 16.8 ?mol/L (all P < 0.05). Besides, IL-6, IL-8, NF-?B, TNF-?, iNOS, ICAM-1, VCAM-1 and COX-2 expressions observed within AD mice models were all beyond those within NC and sham-operated groups (P < 0.05). Also VEGF and HSP 70 were highly expressed within AD mice models than within NC and sham-operated mice (P < 0.05). Transfection of either pcDNA-ANRIL or miR-181b inhibitor could significantly fortify HCAECs' viability and put on their survival rate. At the meantime, the inflammatory factors and vascular-protective parameters were released to a greater level (P < 0.05). Finally, highly expressed ANRIL also notably bring down miR-181b expression and raise p50/p65 expressions within HCAECs (P < 0.05). The joint role of ANRIL, miR-181b and NF-?B signalling could aid in further treating and diagnosing CAD.

SUBMITTER: Guo F

PROVIDER: S-EPMC6156284 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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The interplay of LncRNA ANRIL and miR-181b on the inflammation-relevant coronary artery disease through mediating NF-κB signalling pathway.

Guo Feng F Tang Chengchun C Li Yawei Y Liu Yuqing Y Lv Ping P Wang Wei W Mu Yongyong Y

Journal of cellular and molecular medicine 20180805 10

This study was designed to investigate whether ANRIL affected the aetiology of coronary artery disease (CAD) by acting on downstream miR-181b and NF-κB signalling. Altogether 327 CAD patients diagnosed by angiography were included, and mice models of CAD were established. Human coronary endothelial cells (HCAECs) and human umbilical vein endothelial cells (HUVECs) were also purchased. In addition, shRNA-ANRIL, shRNA-NC, pcDNA3.1-ANRIL, miR-181b mimic, miR-181b inhibitor and miR-NC were transfect ...[more]

PMID: 30079603

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Project description:BackgroundBoth DNA genotype and methylation of antisense non-coding RNA in the INK4 locus (ANRIL) have been robustly associated with coronary artery disease (CAD), but the interdependent mechanisms of genotype and methylation remain unclear.MethodsEighteen tag single nucleotide polymorphisms (SNPs) of ANRIL were genotyped in a matched case-control study (cases 503 and controls 503). DNA methylation of ANRIL and the INK4/ARF locus (p14ARF, p15INK4b and p16INK4a) was measured using pyrosequencing in the same set of samples (cases 100 and controls 100).ResultsPolymorphisms of ANRIL (rs1004638, rs1333048 and rs1333050) were significantly associated with CAD (p < 0.05). The incidence of CAD, multi-vessel disease, and modified Gensini scores demonstrated a strong, direct association with ANRIL gene dosage (p < 0.05). There was no significant association between ANRIL polymorphisms and myocardial infarction/acute coronary syndrome (MI/ACS) (p > 0.05). Methylation levels of ANRIL were similar between the two studied groups (p > 0.05), but were different in the rs1004638 genotype, with AA and AT genotype having a higher level of ANRIL methylation (pos4, p = 0.006; pos8, p = 0.019). Further Spearman analyses indicated that methylation levels of ANRIL were positively associated with systolic blood pressure (pos6, r = 0.248, p = 0.013), diastolic blood pressure (pos3, r = 0.213, p = 0.034; pos6, r = 0.220, p = 0.028), and triglyceride (pos4, r = 0.253, p = 0.013), and negatively associated with high-density lipoprotein cholesterol (pos2, r = - 0.243, p = 0.017). Additionally, we identified 12 transcription factor binding sites (TFBS) within the methylated ANRIL region, and functional annotation indicated these TFBS were associated with basal transcription. Methylation at the INK4/ARF locus was not associated with ANRIL genotype.ConclusionsThese results indicate that ANRIL genotype (tag SNPs rs1004638, rs1333048 and rs1333050) mainly affects coronary atherosclerosis, but not MI/ACS. There may be allele-related DNA methylation and allele-related binding of transcription factors within the ANRIL promoter.

Dataset Information

The interplay of LncRNA ANRIL and miR-181b on the inflammation-relevant coronary artery disease through mediating NF-?B signalling pathway.

Publications

The interplay of LncRNA ANRIL and miR-181b on the inflammation-relevant coronary artery disease through mediating NF-κB signalling pathway.

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