微小RNA-340-5p的过表达改善肺泡II型细胞中的炎症反应和细胞内存活。
Overexpression of microRNA-340-5p Ameliorates Inflammatory Response and Intracellular Survival of in Alveolar Type II Cells.
作者信息
Zhang Bailing, Li Honglang, Zhang Jieling, Hang Yaping, Xu Yi
机构信息
Department of Laboratory Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, People's Republic of China.
Department of Gastrointestinal Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, People's Republic of China.
出版信息
Infect Drug Resist. 2021 Apr 21;14:1573-1584. doi: 10.2147/IDR.S291867. eCollection 2021.
BACKGROUND
The importance of microRNAs (miRs) has been documented in infections. This study estimated the role of miR-340-5p in (Mtb)-infected alveolar type II cells.
METHODS
The microarray of GEO database was analyzed to find the differentially expressed miRs caused by Mtb infection, and miR-340-5p was selected as the research object. The effects of Mtb infection on A549 cells were studied by MTT, CFU, EdU, flow cytometry and ELISA assays. miR-340-5p expression was altered in Mtb-infected A549 cells. The downstream target of miR-340-5p was found by bioinformatics analysis and verified by the rescue experiment. The pathways regulated by miR-340-5p and its target gene were further studied.
RESULTS
Mtb infection suppressed the activity of A549 cells and promoted the release of inflammatory factors. Mtb infection inhibited miR-340-5p expression. Overexpression of miR-340-5p enhanced the resistance of A549 cells to Mtb infection. Moreover, miR-340-5p targeted TMED7. Overexpression of TMED7 reversed the protective effect of miR-340-5p on Mtb-infected A549 cells. miR-340-5p inhibited the activation of NF-κB by targeting TMED7.
CONCLUSION
miR-340-5p inhibits the activation of NF-κB by targeting TMED7, thus alleviating the injury of A549 cells caused by Mtb infection. This study may offer a novel approach to Mtb infection.
背景
微小RNA（miR）在感染中的重要性已被证实。本研究评估了miR-340-5p在结核分枝杆菌（Mtb）感染的II型肺泡细胞中的作用。
方法
分析基因表达综合数据库（GEO数据库）的微阵列，以找出由Mtb感染引起的差异表达miR，并选择miR-340-5p作为研究对象。通过MTT、菌落形成单位（CFU）、5-乙炔基-2'-脱氧尿苷（EdU）、流式细胞术和酶联免疫吸附测定（ELISA）试验研究Mtb感染对A549细胞的影响。在Mtb感染的A549细胞中改变miR-340-5p的表达。通过生物信息学分析找到miR-340-5p的下游靶标，并通过拯救实验进行验证。进一步研究由miR-340-5p及其靶基因调控的信号通路。
结果
Mtb感染抑制A549细胞的活性并促进炎性因子的释放。Mtb感染抑制miR-340-5p的表达。miR-340-5p的过表达增强A549细胞对Mtb感染的抗性。此外，miR-340-5p靶向跨膜蛋白和内质网应激相关蛋白7（TMED7）。TMED7的过表达逆转了miR-340-5p对Mtb感染的A549细胞的保护作用。miR-340-5p通过靶向TMED7抑制核因子κB（NF-κB）的激活。
结论
miR-340-5p通过靶向TMED7抑制NF-κB的激活，从而减轻Mtb感染引起的A549细胞损伤。本研究可能为Mtb感染提供一种新方法。
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