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MicroRNA-182 supplies negative feedback regulation to ameliorate lipopolysaccharide-induced ALI in mice by targeting TLR4.

MicroRNA-182 通过靶向 tlr4 对脂多糖诱导的小鼠 ALI 产生负反馈调节作用。

  • 影响因子:3.89
  • DOI:10.1002/jcp.29504
  • 作者列表:"Yang J","Chen Y","Jiang K","Zhao G","Guo S","Liu J","Yang Y","Deng G
  • 发表时间:2020-01-31
Abstract

:Acute lung injury (ALI), characterized by increased excessive pulmonary inflammation, is a pervasive inflammatory disease with clinically high incidence. MicroRNA (miRNAs) have been associated with the progression of multiple diseases and are regarded as novel regulators of inflammation. However, it remains largely unknown whether the miRNAs-mediated regulatory mechanism has an effect on lipopolysaccharide (LPS)-induced inflammation in ALI. We discovered that miR-182 distinctly lessened expression in the lung tissue of mice with ALI and macrophages stimulated by LPS. We also found that overexpression of miR-182 significantly cut down the secretion of inflammatory cytokines, while this change was reversed by inhibition of miR-182. In addition, miR-182 suppressed the activation of NF-κB by targeting TLR4 expression. And it was confirmed that miR-182 directly regulated TLR4 expression at the posttranscriptional level by binding to the 3'-UTR of TLR4. Together, these data suggested that inhibition of TLR4 expression assuaged LPS-stimulated inflammation through negative feedback regulation of miR-182.

摘要

急性肺损伤 (Acute,ALI) 是临床上发病率较高的一种以过度肺部炎症为特征的炎症性疾病。MicroRNA (miRNAs) 与多种疾病的进展相关,被认为是炎症的新型调节因子。然而,miRNAs 介导的调控机制是否对脂多糖 (LPS) 诱导的 ALI 炎症有影响仍在很大程度上未知。我们发现 miR-182 在 ALI 小鼠肺组织和巨噬细胞中表达明显减少。我们还发现 miR-182 的过表达显著减少了炎性细胞因子的分泌,而这种变化被抑制 miR-182 逆转。此外,miR-182 通过靶向 TLR4 表达抑制 NF-κ b 的活化。并证实 miR-182 通过与 TLR4 的 3 '-UTR 结合,在转录后水平直接调控 TLR4 的表达。总之,这些数据表明,抑制 TLR4 的表达通过负反馈调节 miR-182 缓解 LPS 刺激的炎症。

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DOI:10.1016/j.taap.2019.114847
作者列表:["Bernstein DM","Toth B","Rogers RA","Kling DE","Kunzendorf P","Phillips JI","Ernst H"]

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影响因子:4.04
发表时间:2020-01-10
DOI:10.1042/BST20191010
作者列表:["Zaragosi LE","Deprez M","Barbry P"]

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