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首页> 外文期刊>Cellular Signalling >Up-regulation of microRNA-335-5p reduces inflammation via negative regulation of the TPX2-mediated AKT/GSK3 beta signaling pathway in a chronic rhinosinusitis mouse model
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Up-regulation of microRNA-335-5p reduces inflammation via negative regulation of the TPX2-mediated AKT/GSK3 beta signaling pathway in a chronic rhinosinusitis mouse model

机译：MicroRNA-335-5P的上调通过TPX2介导的AKT /GSK3β信号传导途径的阴性调节在慢性鼻窦炎小鼠模型中减少了炎症

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摘要

Chronic rhinosinusitis (CRS) is featured with chronic symptoms of inflammation or infection in the nasal and sinus tissues. MicroRNAs (miRNAs/miRs), such as dysregulated expression of miR-125b and miR-26a, has been previously demonstrated to be related to CRS. The present study is intended to define the role of miR-335-5p in inflammation and the related mechanism in a mouse model of CRS. The differentially expressed genes associated with CRS were screened by microarray analysis. The targeting relationship between miR-335-5p and TPX2 was analyzed by target prediction program and dual luciferase reporter gene assay. The mouse model of CRS was established, and mice were introduced with miR-335-5p mimics, miR-335-5p inhibitors, or siRNA against TPX2 to explore the regulatory functions of miR-335-5p. The regulatory effect of miR-335-5p on inflammation with the involvement of the AKT signaling pathway was also analyzed with the expression of inflammatory cytokines and AKT signaling pathway-related factors measured. It was indicated that miR-335-5p regulated the TPX2 gene-mediated AKT signaling pathway. TPX2 was identified as a target gene of miR-335-5p, and miR-335-5p elevation inhibited the activation of the AKT signaling pathway. In mice with CRS, up-regulation of miR-335-5p or silence of TPX2 inhibited the inflammation, as evidenced by decreased levels of TNF-alpha, IL-6 and IL-8, and higher levels of GSK3 beta and IL-10. Collectively, miR-335-5p inhibits the activation of AKT signaling pathway by negatively mediating TPX2, which may confer anti-inflammatory protection in CRS.
机译：慢性鼻窦炎（CRS）具有鼻腔和鼻窦组织中急性炎症或感染的慢性症状。 MICRNAS（MIRNAS / MIRS），例如MIR-125B和MIR-26A的失调表达，已经证明与CRS相关。本研究旨在定义MIR-335-5P在CRS小鼠模型中炎症和相关机制的作用。通过微阵列分析筛选与CRS相关的差异表达基因。通过靶预测程序和双荧光素酶报告基因测定分析miR-335-5P和TPX2之间的靶向关系。建立了CRS的小鼠模型，用miR-335-5p模仿，miR-335-5p抑制剂或siRNA引入小鼠，针对TPX2，探讨miR-335-5p的调节功能。炎症细胞因子和AKT信号通路相关因素的表达，还分析了miR-335-5p对Akt信号通路累及的炎症的调节作用。结果表明miR-335-5p调节了TPX2基因介导的AKT信号通路。 TPX2被鉴定为MIR-335-5P的靶基因，MIR-335-5P升高抑制AKT信号通路的激活。在CRS的小鼠中，MIR-335-5P的上调或TPX2的静音抑制了炎症，如TNF-α，IL-6和IL-8水平降低，以及更高水平的GSK3β和IL-10所证明的。统称，MiR-335-5P通过介导TPX2来抑制AKT信号通路的激活，这可能赋予CRS中的抗炎保护。

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