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下调 GAS5 对结核病具有诊断价值,并调节结核分枝杆菌感染的 THP-1 细胞中的炎症反应。

Down-regulation of GAS5 has diagnostic value for tuberculosis and regulates the inflammatory response in mycobacterium tuberculosis infected THP-1 cells.

机构信息

Department of Laboratory Medicine, The Fourth People's Hospital of Huai'an, Jiangsu, 223001, China.

School of Medical Technology, Jiangsu College of Nursing, Jiangsu, 223007, China.

出版信息

Tuberculosis (Edinb). 2022 Jan;132:102141. doi: 10.1016/j.tube.2021.102141. Epub 2021 Nov 15.

DOI:10.1016/j.tube.2021.102141
PMID:34808575
Abstract

OBJECTIVE

This study aimed to investigate the expression of long non-coding RNA (lncRNA) growth arrest-special transcript 5 (GAS5) in the serum of tuberculosis (TB) patients and discuss the mechanism of GAS5 in TB by establishing an in-vitro TB cell model.

METHODS

Serum expressions of GAS5 and miR-18a-5p were determined by quantitative real-time PCR (qRT-PCR). The effects of GAS5 on macrophage cell viability and the inflammatory response after MTB infection were assessed by CCK-8 and ELISA. Luciferase reporter gene assay was applied to delve into the potential target gene of GAS5.

RESULTS

The expression of GAS5 in TB patients was down-regulated, while miR-18a-5p was up-regulated, and the serum inflammatory factors were negatively correlated with the expression level of GAS5. MTB infection induced significant upregulation on the cell viability and inflammatory response but the acceleration effect could be rescued by GAS5-overexpression. Meanwhile, miR-18a-5p was recognized as the target gene of GAS5.

CONCLUSION

This study indicated that the expression level of GAS5 in the serum of TB patients was decreased, while in the cells infected with MTB, the down-regulated GAS5 might develop a role in facilitating the cell vitality and the inflammatory response by adsorbing miR-18a-5p in the form of molecular sponge.

摘要

目的

本研究旨在探讨长链非编码 RNA(lncRNA)生长停滞特异性转录本 5(GAS5)在结核病(TB)患者血清中的表达,并通过建立体外 TB 细胞模型探讨 GAS5 在 TB 中的作用机制。

方法

采用实时荧光定量 PCR(qRT-PCR)检测 GAS5 和 miR-18a-5p 的血清表达。通过 CCK-8 和 ELISA 评估 GAS5 对 MTB 感染后巨噬细胞活力和炎症反应的影响。应用荧光素酶报告基因检测深入探讨 GAS5 的潜在靶基因。

结果

TB 患者血清中 GAS5 的表达下调,而 miR-18a-5p 上调,且血清炎症因子与 GAS5 表达水平呈负相关。MTB 感染诱导细胞活力和炎症反应显著上调,但 GAS5 过表达可挽救这种加速作用。同时,miR-18a-5p 被鉴定为 GAS5 的靶基因。

结论

本研究表明,TB 患者血清中 GAS5 的表达水平降低,而在感染 MTB 的细胞中,下调的 GAS5 可能通过吸附 miR-18a-5p 形成分子海绵的形式发挥促进细胞活力和炎症反应的作用。

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