Open Access

MicroRNA‑21 inhibits lipopolysaccharide‑induced acute lung injury by targeting nuclear factor‑κB

  • Authors:
    • Wei‑Dong Zhu
    • Jia Xu
    • Mao Zhang
    • Tie‑Ming Zhu
    • Yun‑Hua Zhang
    • Ke Sun
  • View Affiliations

  • Published online on: September 24, 2018     https://doi.org/10.3892/etm.2018.6789
  • Pages: 4616-4622
  • Copyright: © Zhu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute lung injury (ALI) is a frequent, but severe complication following sepsis in patients with critical illness. The present study aimed to investigate the potential role of microRNA‑21 (miR‑21) in the regulation of inflammation in the ALI induced by lipopolysaccharide (LPS) in vitro and in vivo. The levels of inflammatory cytokines, tumor necrosis factor (TNF)‑α, interleukin (IL)‑6, IL‑1β and IL‑10, and the level of miR‑21 expression were measured in the lungs of LPS‑induced ALI rats and NR8383 alveolar macrophages (AMs). To confirm the regulatory effect of miR‑21 in the inflammatory reactions of ALI, NR8383 cells were transfected with a mimic of miR‑21 or an anti‑miR‑21 inhibitor, and the subsequent changes of the miR‑21 level and the levels of inflammatory cytokines were detected. The underlying molecular mechanism was also investigated. LPS‑induced ALI in rats resulted in significant overexpression of pro‑inflammatory cytokines, TNF‑α, IL‑6 and IL‑1β, and miR‑21, but reduced the expression of the anti‑inflammatory cytokine IL‑10. LPS treatment also led to a higher expression level of miR‑21 and increased secretion of pro‑inflammatory cytokines in NR8383 cells in a time‑dependent manner. Manipulation with the miR‑21 mimic significantly suppressed the LPS‑mediated induction of TNF‑α, IL‑6 and IL‑1β in NR8383 cells, while that induction was upregulated when miR‑21 expression was silenced via transfection with the anti‑miR‑21 inhibitor. Further mechanism experiments revealed that miR‑21 regulates LPS‑induced inflammation responses via the Toll‑like receptor 4 and nuclear factor‑κB (Nf‑κB) signaling pathway. miR‑21 negatively regulates inflammatory responses in LPS‑induced ALI by targeting the NF‑κB signaling pathway, providing further insight into the molecular mechanism of ALI progression.
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December-2018
Volume 16 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Copy and paste a formatted citation
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Spandidos Publications style
Zhu WD, Xu J, Zhang M, Zhu TM, Zhang YH and Sun K: MicroRNA‑21 inhibits lipopolysaccharide‑induced acute lung injury by targeting nuclear factor‑κB. Exp Ther Med 16: 4616-4622, 2018.
APA
Zhu, W., Xu, J., Zhang, M., Zhu, T., Zhang, Y., & Sun, K. (2018). MicroRNA‑21 inhibits lipopolysaccharide‑induced acute lung injury by targeting nuclear factor‑κB. Experimental and Therapeutic Medicine, 16, 4616-4622. https://doi.org/10.3892/etm.2018.6789
MLA
Zhu, W., Xu, J., Zhang, M., Zhu, T., Zhang, Y., Sun, K."MicroRNA‑21 inhibits lipopolysaccharide‑induced acute lung injury by targeting nuclear factor‑κB". Experimental and Therapeutic Medicine 16.6 (2018): 4616-4622.
Chicago
Zhu, W., Xu, J., Zhang, M., Zhu, T., Zhang, Y., Sun, K."MicroRNA‑21 inhibits lipopolysaccharide‑induced acute lung injury by targeting nuclear factor‑κB". Experimental and Therapeutic Medicine 16, no. 6 (2018): 4616-4622. https://doi.org/10.3892/etm.2018.6789