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高表达的长非编码RNA SNHG14通过向miR-223-3p激活MSU诱导的炎症反应在急性痛风关节炎中

Lu Yang¹, Xiaochuan Liu¹, Shuyi Yan¹

¹Clinical Research Center, Shanghai Baoshan Luodian Hospital, Shanghai, China.

International journal of rheumatic diseases

|September 16, 2023

概括

长非编码RNA SNHG14在急性痛风性关节炎 (AGA) 中升高,并通过海绵miR-223-3p促进炎症. 沉默SNHG14或过度表达miR-223-3p可以缓解AGA的炎症反应.

科学领域:

生物化学生物化学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

长非编码RNAs (lncRNAs) 与炎症性疾病的发生有关.
在急性痛风性关节炎 (AGA) 中,特定的lncRNAs (如SNHG14) 的作用尚未完全阐明.

研究的目的:

在患有AGA的患者中研究lncRNA SNHG14的表达水平.
探索lncRNA SNHG14在调节AGA中的炎症反应中的潜在机制.

主要方法:

使用定量实时PCR (qRT-PCR) 来测量lncRNA SNHG14表达.
在实验室中,使用用单酸盐 (MSU) 刺激的THP-1细胞建立了AGA的细胞模型.
与酶相关的免疫吸收试验 (ELISA) 量化了炎症性细胞因子; luciferase 记者试验验证了 SNHG14 和 miR-223-3p 之间的相互作用.

主要成果:

与对照组相比,AGA患者的lncRNA SNHG14血清水平明显高于对照组,显示出诊断潜力.
抑制SNHG14可以减少THP-1细胞中MSU诱导的炎症.
SNHG14直接与miR-223-3p结合,在AGA患者和细胞模型中,miR-223-3p水平下降.

结论:

在AGA的背景下, lncRNA SNHG14充当了miR-223-3p的分子海绵.
这种相互作用通过调节miR-223-3p水平来促进细胞炎症反应,从而加剧了AGA进展.

关键词:

剧烈的痛风性关节炎炎症反应是一种炎症反应.长非编码RNASNHG14是SNHG14的编码.在 miR-223-3p 中使用.

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lncRNA - Long Non-coding RNAs

lncRNA - Long Non-coding RNAs

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MicroRNAs

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