Circ_0026579 alleviates LPS-induced WI-38 cells inflammation injury in infantile pneumonia.

IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yang Yu, Tingting Yang, Zhaozheng Ding, Yuan Cao
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引用次数: 9

Abstract

Circular RNA (circRNA) represents an important regulator in infantile pneumonia progression. To clarify the role of circ_0026579 in this disease, LPS was used to treat WI-38 cells to mimic inflammation injury. The levels of inflammatory factors were determined by ELISA assay. Cell proliferation and apoptosis were measured by MTT assay, EdU staining and flow cytometry. The protein levels of cyclinD1, cleaved-caspase-3 and insulin-like growth factor 2 (IGF2) were examined using Western blot analysis. Cell oxidative stress was assessed by detecting MDA level and SOD activity. The expression of circ_0026579, miR-24-3p and IGF2 were analyzed using quantitative real-time PCR, and the interaction between miR-24-3p and circ_0026579 or IGF2 was confirmed by dual-luciferase reporter assay and RIP assay. LPS induced inflammation in WI-38 cells. Circ_0026579 expression was promoted in LPS-induced WI-38 cells, and its knockdown alleviated LPS-induced WI-38 cells inflammation. MiR-24-3p was sponged by circ_0026579, and its expression was reduced by LPS. MiR-24-3p inhibitor reversed the regulation of circ_0026579 knockdown on LPS-induced WI-38 cells inflammation. IGF2 was targeted by miR-24-3p, and its expression could be enhanced by LPS. MiR-24-3p relieved the inflammation of WI-38 cells which could be abolished by IGF2 overexpression. Circ_0026579 positively regulated IGF2 expression through sponging miR-24-3p. Circ_0026579 knockdown alleviated LPS-induced WI-38 cells inflammation by miR-24-3p/IGF2 axis, suggesting that circ_0026579 might contribute to infantile pneumonia progression.

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Circ_0026579减轻lps诱导的婴儿肺炎WI-38细胞炎症损伤。
环状RNA (circRNA)是婴儿肺炎进展的重要调节因子。为了阐明circ_0026579在该疾病中的作用,我们使用LPS治疗WI-38细胞来模拟炎症损伤。ELISA法检测各组炎症因子水平。采用MTT法、EdU染色法和流式细胞术检测细胞增殖和凋亡。Western blot检测cyclinD1、cleaved-caspase-3和胰岛素样生长因子2 (IGF2)蛋白水平。通过检测MDA水平和SOD活性评估细胞氧化应激。采用实时荧光定量PCR分析circ_0026579、miR-24-3p和IGF2的表达,并通过双荧光素酶报告基因实验和RIP实验证实miR-24-3p与circ_0026579或IGF2的相互作用。LPS诱导WI-38细胞炎症。Circ_0026579在lps诱导的WI-38细胞中表达增强,敲低Circ_0026579可减轻lps诱导的WI-38细胞炎症。用circ_0026579擦拭MiR-24-3p, LPS降低其表达。MiR-24-3p抑制剂逆转circ_0026579敲低对lps诱导的WI-38细胞炎症的调节。IGF2被miR-24-3p靶向,LPS可增强其表达。MiR-24-3p可减轻WI-38细胞的炎症反应,而IGF2过表达可消除炎症反应。Circ_0026579通过海绵组织miR-24-3p正向调节IGF2的表达。Circ_0026579敲低可通过miR-24-3p/IGF2轴减轻lps诱导的WI-38细胞炎症,提示Circ_0026579可能参与婴儿肺炎进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Innate Immunity
Innate Immunity 生物-免疫学
CiteScore
7.20
自引率
0.00%
发文量
20
审稿时长
6-12 weeks
期刊介绍: Innate Immunity is a highly ranked, peer-reviewed scholarly journal and is the official journal of the International Endotoxin & Innate Immunity Society (IEIIS). The journal welcomes manuscripts from researchers actively working on all aspects of innate immunity including biologically active bacterial, viral, fungal, parasitic, and plant components, as well as relevant cells, their receptors, signaling pathways, and induced mediators. The aim of the Journal is to provide a single, interdisciplinary forum for the dissemination of new information on innate immunity in humans, animals, and plants to researchers. The Journal creates a vehicle for the publication of articles encompassing all areas of research, basic, applied, and clinical. The subject areas of interest include, but are not limited to, research in biochemistry, biophysics, cell biology, chemistry, clinical medicine, immunology, infectious disease, microbiology, molecular biology, and pharmacology.
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