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MiR-222-3p ameliorates glucocorticoid-induced inhibition of airway epithelial cell repair through down-regulating GILZ expression
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-03-21 , DOI: 10.1080/10799893.2020.1742739
Ning He 1 , Liping Liu 1 , Juan Ding 1 , Yuemei Sun 1 , Haiyan Xing 1 , Shuyun Wang 1
Affiliation  

Abstract GILZ expression is induced by glucocorticoids (GCs) and is involved in the mechanism of airway epithelial cell repair in patients with asthma. The present study aimed to investigate the role of miR-222-3p/GILZ pathway in treatment of airway epithelial cell repair by GCs. 9HTE cells were treated by 10 µmol/L dexamethasone (Dex) for 6, 12, and 24 hours (h). MiR-222-3p mimic and GILZ were used for cell transfection. Cell vitality, migration, and invasion were detected by methyl-thiazolyl tetrazolium (MTT), wound healing, and Transwell. The targeting relationship between miR-222-3p and GILZ was predicted by TargetScan and further confirmed by dual-luciferase reporter assay. The expressions of relative mRNAs or proteins were detected by Western blot and quantitative polymerase chain reaction (qPCR). The results showed that Dex treatment up-regulated the GILZ expression level but inhibited the levels of p-Raf1, p-MEK1/2, p-ERK1/2, and miR-222-3p of the cells, moreover, it also inhibited cell activity, migration, and invasion in a time-dependent manner. MiR-222-3p specifically targeted GILZ. MiR-222-3p mimic ameliorated the cell viability, migration, and invasion reduced by Dex treatment, increased the expression levels of p-Raf1 and p-MEK1/2, p-ERK1/2, and partially reversed the effects of GILZ overexpression on the above indexes. Moreover, GILZ showed the opposite effects to miR-222-3p. MiR-222-3p activated MAPK signaling pathway through inhibiting the GILZ expression, thus promoting the cell viability, migration, and invasion previously reduced by Dex.

中文翻译:

MiR-222-3p 通过下调 GILZ 表达改善糖皮质激素诱导的气道上皮细胞修复抑制

摘要 GILZ 表达由糖皮质激素(GCs)诱导,参与哮喘患者气道上皮细胞修复的机制。本研究旨在探讨miR-222-3p/GILZ通路在GCs治疗气道上皮细胞修复中的作用。9HTE 细胞用 10 µmol/L 地塞米松 (Dex) 处理 6、12 和 24 小时 (h)。MiR-222-3p 模拟物和 GILZ 用于细胞转染。通过甲基噻唑基四唑 (MTT)、伤口愈合和 Transwell 检测细胞活力、迁移和侵袭。miR-222-3p 和 GILZ 之间的靶向关系由 TargetScan 预测,并通过双荧光素酶报告基因检测进一步证实。通过蛋白质印迹和定量聚合酶链反应(qPCR)检测相关mRNA或蛋白质的表达。结果表明,Dex 处理上调 GILZ 表达水平,但抑制细胞的 p-Raf1、p-MEK1/2、p-ERK1/2 和 miR-222-3p 的水平,此外,它还抑制细胞以时间依赖的方式活动、迁移和入侵。MiR-222-3p 专门针对 GILZ。MiR-222-3p 模拟物改善了 Dex 处理降低的细胞活力、迁移和侵袭,增加了 p-Raf1 和 p-MEK1/2、p-ERK1/2 的表达水平,并部分逆转了 GILZ 过表达对以上指标。此外,GILZ 显示出与 miR-222-3p 相反的效果。MiR-222-3p 通过抑制 GILZ 表达激活 MAPK 信号通路,从而促进先前被 Dex 降低的细胞活力、迁移和侵袭。和细胞的 miR-222-3p,此外,它还以时间依赖性方式抑制细胞活性、迁移和侵袭。MiR-222-3p 专门针对 GILZ。MiR-222-3p 模拟物改善了 Dex 处理降低的细胞活力、迁移和侵袭,增加了 p-Raf1 和 p-MEK1/2、p-ERK1/2 的表达水平,并部分逆转了 GILZ 过表达对以上指标。此外,GILZ 显示出与 miR-222-3p 相反的效果。MiR-222-3p 通过抑制 GILZ 表达激活 MAPK 信号通路,从而促进先前被 Dex 降低的细胞活力、迁移和侵袭。和细胞的 miR-222-3p,此外,它还以时间依赖性方式抑制细胞活性、迁移和侵袭。MiR-222-3p 专门针对 GILZ。MiR-222-3p 模拟物改善了 Dex 处理降低的细胞活力、迁移和侵袭,增加了 p-Raf1 和 p-MEK1/2、p-ERK1/2 的表达水平,并部分逆转了 GILZ 过表达对以上指标。此外,GILZ 显示出与 miR-222-3p 相反的效果。MiR-222-3p 通过抑制 GILZ 表达激活 MAPK 信号通路,从而促进先前被 Dex 降低的细胞活力、迁移和侵袭。Dex处理降低和侵袭,增加了p-Raf1和p-MEK1/2、p-ERK1/2的表达水平,部分逆转了GILZ过表达对上述指标的影响。此外,GILZ 显示出与 miR-222-3p 相反的效果。MiR-222-3p 通过抑制 GILZ 表达激活 MAPK 信号通路,从而促进先前被 Dex 降低的细胞活力、迁移和侵袭。Dex处理降低和侵袭,增加了p-Raf1和p-MEK1/2、p-ERK1/2的表达水平,部分逆转了GILZ过表达对上述指标的影响。此外,GILZ 显示出与 miR-222-3p 相反的效果。MiR-222-3p 通过抑制 GILZ 表达激活 MAPK 信号通路,从而促进先前被 Dex 降低的细胞活力、迁移和侵袭。
更新日期:2020-03-21
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