Yang Lu, Liu Xiaochuan, Yan Shuyi, Xiong Shili, Bai Xiaosong, Yan Ying
Clinical Research Center, Shanghai Baoshan Luodian Hospital, Shanghai, China.
Department of Clinical Laboratory, Shanghai Baoshan Luodian Hospital, Shanghai, China.
Int J Rheum Dis. 2023 Nov;26(11):2233-2239. doi: 10.1111/1756-185X.14919. Epub 2023 Sep 15.
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.
据报道，长链非编码RNA（lncRNA）参与多种炎症性疾病的调控。在此，我们的主要目的是确定lncRNA SNHG14在急性痛风性关节炎（AGA）中的表达数据，并探讨其在AGA调控中的可能机制。
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以评估lncRNA SNHG14在AGA诊断中的准确性。通过用尿酸钠（MSU）诱导THP-1细胞构建体外AGA细胞模型。采用酶联免疫吸附测定法检测白细胞介素-1β、白细胞介素-6和肿瘤坏死因子-α等炎症因子的浓度。利用荧光素酶报告基因验证lncRNA SNHG14与miR-223-3p之间的关系。
临床分析中，AGA患者血清lncRNA SNHG14水平显著高于对照组。lncRNA SNHG14异常升高对AGA诊断具有高敏感性和特异性。体外细胞实验中，沉默lncRNA SNHG14可抑制MSU刺激的THP-1细胞的炎症反应，荧光素酶报告基因证明lncRNA SNHG14可与miR-223-3p结合。此外，AGA患者和AGA细胞模型中miR-223-3p水平下降。miR-223-3p过表达有助于减轻MSU诱导的炎症反应。
在AGA细胞模型中，lncRNA SNHG14作为miR-223-3p的海绵，通过控制miR-223-3p水平诱导细胞炎症反应，从而加重AGA的疾病进展。
