LncRNA AC040162.3通过miRNA-223-3p/NLRP3分子轴促进hcv诱导的T2DM恶化。

IF 2.6 4区 医学 Q3 CELL BIOLOGY
Ben Niu, Xueshan Xia, Lijing Ma, Lixuan Yao, Yating Zhang, Heng Su
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引用次数: 0

摘要

背景:糖尿病是世界范围内最常见的疾病之一,也是主要的公共卫生负担。2型糖尿病(T2DM)与慢性丙型肝炎病毒(HCV)感染相关,lncrna在HCV诱导的T2DM中发挥重要作用。我们旨在探讨lncRNA AC040162.3对hcv诱导的T2DM的影响。方法:采用HCV感染MIN6细胞建立体外模型。采用实时定量PCR (RT-qPCR)检测HCV拷贝数和miRNA表达。采用酶联免疫吸附法(ELISA)检测胰岛素分泌,甲基噻唑四氮唑(MTT)检测细胞活力。Western blotting和流式细胞术分析细胞凋亡。此外,使用Western blotting和tdt介导的dUTP Nick End Labeling (TUNEL)分析焦亡。荧光素酶报告基因检测用于研究靶向关系。结果:在HCV-T2DM中,LncRNA AC040162.3和NLRP3的表达明显升高,miR-223-3p的表达明显抑制。体外实验表明,lncRNA AC040162.3沉默或miR-223-3p过表达可通过抑制细胞凋亡和焦亡,增强细胞活力,显著缓解hcv诱导的T2DM恶化。然后,我们证明沉默lncRNA AC040162.3促进了miR-223-3p的表达,并且miR-223-3p结合到lncRNA AC040162.3和NLRP3结合位点。此外,LncRNA AC040162.3沉默在hcv感染的MIN6细胞中的保护作用被NLRP3过表达或miR-223-3p沉默逆转。结论:沉默lncRNA AC040162.3可通过调控miR-223-3p/NLRP3轴缓解hcv诱导的T2DM过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

LncRNA AC040162.3 Promotes HCV-Induced T2DM Deterioration through the miRNA-223-3p/NLRP3 Molecular Axis.

LncRNA AC040162.3 Promotes HCV-Induced T2DM Deterioration through the miRNA-223-3p/NLRP3 Molecular Axis.

LncRNA AC040162.3 Promotes HCV-Induced T2DM Deterioration through the miRNA-223-3p/NLRP3 Molecular Axis.

LncRNA AC040162.3 Promotes HCV-Induced T2DM Deterioration through the miRNA-223-3p/NLRP3 Molecular Axis.

Background: Diabetes is one of the most common diseases and major public health burdens worldwide. Type 2 diabetes mellitus (T2DM) is associated with chronic hepatitis C virus (HCV) infection, and lncRNAs play an important role in HCV-induced T2DM. We aimed to explore the effect of lncRNA AC040162.3 on HCV-induced T2DM.

Methods: HCV was used to infect MIN6 cells to establish an in vitro model. HCV copy number and miRNA expression were detected by Real Time Quantitative PCR (RT-qPCR). Enzyme-Linked Immunosorbent Assay (ELISA) was used to detect the secretion of insulin, and methyl thiazolyl tetrazolium (MTT) was applied to analyze cell viability. Apoptosis was analyzed by Western blotting and flow cytometry. In addition, Western blotting and TdT-mediated dUTP Nick End Labeling (TUNEL) were used to analyze pyroptosis. Luciferase reporter assays were used to investigate the targeting relationship.

Results: The expression of LncRNA AC040162.3 and NLRP3 was markedly increased in HCV-T2DM, while the expression of miR-223-3p was remarkably inhibited. In vitro experiments demonstrated that lncRNA AC040162.3 silencing or miR-223-3p overexpression remarkably alleviated HCV-induced T2DM deterioration by inhibiting cell apoptosis and pyroptosis and enhancing cell viability. We then demonstrated that silencing lncRNA AC040162.3 promoted the expression of miR-223-3p and that miR-223-3p bound to lncRNA AC040162.3 and the NLRP3 binding site. In addition, the protective effects of LncRNA AC040162.3 silencing in HCV-infected MIN6 cells were reversed by overexpression of NLRP3 or silencing of miR-223-3p.

Conclusion: Silencing of lncRNA AC040162.3 alleviates the process of HCV-induced T2DM by governing the miR-223-3p/NLRP3 axis.

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来源期刊
Analytical Cellular Pathology
Analytical Cellular Pathology ONCOLOGY-CELL BIOLOGY
CiteScore
4.90
自引率
3.10%
发文量
70
审稿时长
16 weeks
期刊介绍: Analytical Cellular Pathology is a peer-reviewed, Open Access journal that provides a forum for scientists, medical practitioners and pathologists working in the area of cellular pathology. The journal publishes original research articles, review articles, and clinical studies related to cytology, carcinogenesis, cell receptors, biomarkers, diagnostic pathology, immunopathology, and hematology.
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