Highly expressed long non‐coding RNA SNHG14 activated MSU‐induced inflammatory response in acute gout arthritis through targeting miR‐223‐3p

Abstract

AbstractAimAccording to reports, long non‐coding RNAs (lncRNAs) are involved in the regulation of many inflammatory diseases. Here, our main purpose was to ascertain the expression data of lncRNA SNHG14 in acute gouty arthritis (AGA) and to explore its possible mechanism in the regulation of AGA.MethodReverse transcription quantitative polymerase chain reaction technology was supplied to detect the lncRNA SNHG14 expression. A receiver operating characteristics curve was drawn to estimate the accuracy of lncRNA SNHG14 in AGA diagnosis. An in vitro AGA cell model was constructed by inducing THP‐1 cells with monosodium urate (MSU). The concentrations of inflammatory factors such as interleukin‐1β, interleukin‐6, and tumor necrosis factor‐α were measured by enzyme‐linked immunosorbent assay. The luciferase reporter gene was used to verify the relationship between lncRNA SNHG14 and miR‐223‐3p.ResultsIn clinical analysis, the levels of serum lncRNA SNHG14 in AGA patients were significantly higher than those in the control group. Abnormally elevated lncRNA SNHG14 has high sensitivity and specificity for AGA diagnosis. In in vitro cell experiments, silencing lncRNA SNHG14 inhibited the inflammatory response of THP‐1 cells stimulated by MSU, and the luciferase reporter gene proved that lncRNA SNHG14 could bind to miR‐223‐3p. In addition, the level of miR‐223‐3p declined in AGA patients and the AGA cell model. Overexpression of miR‐223‐3p is helpful to alleviate an MSU‐induced inflammatory response.ConclusionIn the AGA cell model, lncRNA SNHG14, as an miR‐223‐3p sponge, induces a cellular inflammatory response by controlling the level of miR‐223‐3p, so aggravating the disease progress of AGA.