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The anti‐inflammatory effect of microRNA‐383‐3p interacting with IL1R2 against homocysteine‐induced endothelial injury in rat coronary arteries

MicroRNAs (miRs) are widely reported to be novel biomarkers involved in the process of coronary atherosclerosis (CAS). Hence, this study aims to explore the function of miR‐383‐3p targeting IL1R2 on inflammatory injury of coronary artery endothelial cells (CAECs) in CAS. The underlying regulatory mechanisms of miR‐383‐3p were analyzed in concert with the treatment of miR‐383‐3p mimics, miR‐383‐3p inhibitors, and the combination of miR‐383‐3p inhibitors and siRNA against IL1R2 in homocysteine (HCY)‐induced CAECs. MTT, Hoechst 33258 staining, and tube formation assay were employed in order to measure cell viability, apoptosis, and tube formation, respectively. The levels of IL‐1β, IL‐6, IL‐10, and IL‐18 were determined by ELISA. IL1R2 was verified as the target gene of miR‐383‐3p by dual‐luciferase reporter gene assay. MiR‐383‐3p was down‐regulated in myocardial tissues of AS rats while IL1R2 was the reciprocal. The up‐regulation of miR‐383‐3p decreased the levels of IL1R2, caspase‐1, IL‐1β, IL‐6, and IL‐18 expressions, as well as cell apoptosis rate in the HCY‐induced CAECs, while IL‐10 expression, cell viability, and tube formation ability were increased. These results were contraindicated in the HCY‐induced CAECs treated by miR‐383‐3p inhibitors. In conclusion, miR‐383‐3p mediating IL1R2 prevents HCY‐induced apoptosis and inflammation injury in CAECs through the inhibition of the activation of inflammasome signaling pathway. These findings highly indicate that miR‐383‐3p may be beneficial in the prevention of CAS and other cardiovascular diseases.