The interplay of LncRNA ANRIL and miR‐181b on the inflammation‐relevant coronary artery disease through mediating NF‐κB 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‐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 transfected into the cells. The lipopolysaccharides (LPS) and pyrrolidine dithiocarbamate (PDTC) were also added to activate or deactivate NF‐κB 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 μmol/L (all P < 0.05). Besides, IL‐6, IL‐8, NF‐κB, TNF‐α, 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‐κB signalling could aid in further treating and diagnosing CAD.

Long Non-Coding RNAs Link Oxidized Low-Density Lipoprotein With the Inflammatory Response of Macrophages in Atherogenesis

“…In contrast, ANRIL was also found to promote the lipid uptake and cholesterol transport in THP-1 macrophage-derived foam cells and mouse models by regulating the CDKN2B promoter (67,68). ANRIL promotes LPS induced-inflammation in human coronary artery endothelial cells (HCAECs) and human umbilical vein endothelial cells (HUVECs) via sponging miR-181b and then activating NF-κB signaling in vitro (69). Similarly, ANRIL induced by TNF-α also promoted inflammatory cytokines such as IL-6 or IL-8 in ECs through activation of NF-κB (70).…”

A novel plasma lncRNA ENST00000416361 is upregulated in coronary artery disease and is related to inflammation and lipid metabolism

“…The c allele of rs1800795 is located on the il-6 gene promoter, and IL-6 rs1800795-tobacco smoking and IL-6 rs1800795-alcohol consumption interactions have been associated with increased cad risk (41). lncrna anril affects the progression of CAD by targeting miR-181b, activating the nF-κB signal pathway and inducing the release of inflammatory factors such as il-6 and TnF-α (42).…”

Translational Genomics in Neurocritical Care: a Review

“…Although the direct impact of these variants in human tissue or animal models is difficult to discern, work with mutations of ANRIL in endothelial models have provided valuable insight. Specifically, upregulation of ANRIL has been associated with increased expression of inflammatory and oxidative markers in the vascular tissue such as IL-6, IL-8, NF-κB, TNF-a, iNOS, ICAM-1, VCAM-1, and COX-2 (130,131). These observations provide vital information about cellular mechanisms impacted by human disease-associated genetic risk factors without requiring the expense and time investment of creating, validating, and studying animal models.…”