高表达的长链非编码RNA SNHG14 通过靶向miR-223-3p激活了急性痛风性关节炎中MSU诱导的炎症反应。
Highly expressed long non-coding RNA SNHG14 activated MSU-induced inflammatory response in acute gout arthritis through targeting miR-223-3p.
发表日期:2023 Sep 15
作者:
Lu Yang, Xiaochuan Liu, Shuyi Yan, Shili Xiong, Xiaosong Bai, Ying Yan
来源:
ARTHRITIS RESEARCH & THERAPY
摘要:
根据报道,长链非编码RNA(lncRNA)参与了许多炎症性疾病的调节。在这里,我们的主要目的是确定急性痛风性关节炎(AGA)中lncRNA SNHG14的表达数据,并探索其在AGA调节中的可能机制。采用逆转录定量聚合酶链反应技术检测lncRNA SNHG14的表达。绘制受试者工作特征曲线来评估lncRNA SNHG14在AGA诊断中的准确性。通过用单一钠尿酸(MSU)诱导THP-1细胞建立体外AGA细胞模型。通过酶联免疫吸附测定法测量白细胞介素-1β、白细胞介素-6和肿瘤坏死因子-α等炎性因子的浓度。使用荧光素酶报告基因验证lncRNA SNHG14与miR-223-3p的关系。在临床分析中,AGA患者血清lncRNA SNHG14水平显著高于对照组。异常升高的lncRNA SNHG14对AGA诊断具有较高的敏感性和特异性。在体外细胞实验中,沉默lncRNA SNHG14抑制了MSU刺激下THP-1细胞的炎症反应,并且荧光素酶报告基因证实了lncRNA SNHG14能够结合miR-223-3p。此外,miR-223-3p水平在AGA患者和AGA细胞模型中下降。miR-223-3p的过表达有助于缓解MSU诱导的炎症反应。在AGA细胞模型中,作为miR-223-3p海绵体的lncRNA SNHG14通过控制miR-223-3p的水平诱导细胞炎症反应,从而加重AGA疾病进展。
© 2023亚太风湿病协会联盟和John Wiley & Sons Australia有限公司。
According 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.Reverse 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.In 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.In 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.© 2023 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd.