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PVT1 敲低通过调节 miR-24 抑制 LPS 诱导的心肌成纤维细胞的生物学行为。

PVT1 knockdown inhibited the biological behavior of LPS-induced cardiac fibroblasts by regulating miR-24.

机构信息

Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, No.137, Liyushan South Road, Xincheng District, Xinjiang Uygur Autonomous Region, Urumqi, 830054, China.

出版信息

Genes Genomics. 2021 Sep;43(9):1003-1009. doi: 10.1007/s13258-021-01104-0. Epub 2021 Apr 27.

DOI:10.1007/s13258-021-01104-0
PMID:33907980
Abstract

BACKGROUND

The heart is one of the target organs vulnerable to sepsis. About 50% of sepsis patients will suffer from myocardial injury and cardiac dysfunction, which will aggravate the sepsis and affect its prognosis.

OBJECTIVES

Here, we attempt to investigate the function of long non coding RNA PVT1 in LPS-induced cardiac fibroblasts in vitro, and explore its potential mechanism.

METHODS

The expression of PVT1 in LPS-induced cardiac fibroblasts was detected by qRT-PCR. CCK-8 assay, cell migration, qRT-PCR and western blotting analysis were applied to evaluating the effect of PVT1 knockdown on LPS-induced cardiac fibroblasts. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism.

RESULTS

PVT1 expression was up-regulated in LPS-induced cardiac fibroblasts. And knockdown of PVT1 inhibited cell viability and migration, alleviated inflammation cytokines production of LPS-treated cardiac fibroblasts. The bioinformatics analysis predicted PVT1 negatively regulates miR-24 and KLF6 is a direct target of miR-24.

CONCLUSIONS

In a word, we observed PVT1 expression level was up-regulated in LPS- treated cardiac fibroblasts. PVT1 knockdown could alleviate LPS-induced biological behavior of cardiac fibroblasts through sponging miR-24 in vitro.

摘要

背景

心脏是易受脓毒症影响的靶器官之一。约 50%的脓毒症患者会发生心肌损伤和心功能障碍,这将加重脓毒症并影响其预后。

目的

本研究旨在探讨长链非编码 RNA PVT1 在 LPS 诱导的心肌成纤维细胞中的作用及其潜在机制。

方法

通过 qRT-PCR 检测 LPS 诱导的心肌成纤维细胞中 PVT1 的表达。通过 CCK-8 测定、细胞迁移实验、qRT-PCR 和 Western blot 分析评估 PVT1 敲低对 LPS 诱导的心肌成纤维细胞的影响。通过生物信息学分析和挽救实验探讨其潜在机制。

结果

PVT1 在 LPS 诱导的心肌成纤维细胞中表达上调。敲低 PVT1 抑制 LPS 处理的心肌成纤维细胞的细胞活力和迁移,减轻炎症细胞因子的产生。生物信息学分析预测 PVT1 负调控 miR-24,KLF6 是 miR-24 的直接靶基因。

结论

总之,我们观察到 LPS 处理的心肌成纤维细胞中 PVT1 的表达水平上调。PVT1 敲低可通过体外海绵吸附 miR-24 减轻 LPS 诱导的心肌成纤维细胞的生物学行为。

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