Open Access

Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression

  • Authors:
    • Jianan Chen
    • Xingsheng Gu
    • Li Zhou
    • Shuguang Wang
    • Limei Zhu
    • Yangneng Huang
    • Feng Cao
  • View Affiliations

  • Published online on: September 27, 2019     https://doi.org/10.3892/etm.2019.8063
  • Pages: 3959-3967
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Sepsis remains the primary cause of death in intensive care units and multiple long non‑coding RNAs (lncRNAs) have been demonstrated to be dysregulated in samples of patients with sepsis. However, whether lncRNA‑HOTAIR is involved in the etiology of sepsis remains unclear. The aim of the present study was to investigate the role of HOTAIR in sepsis and to reveal the associated mechanisms. A bioinformatics analysis and dual‑luciferase reporter assay was performed to evaluate the interaction between HOTAIR and miR‑211, as well as miR‑211 and IL‑6R. An animal model of sepsis was established in mice via cecal ligation and puncture. Interferon (IFN)‑γ, interleukin (IL)‑6, IL‑17, tumor necrosis factor (TNF)‑α, IL‑1β, IL‑6 receptor (R), microRNA (miR)‑211 and HOTAIR expression was measured using reverse transcription‑quantitative PCR. Cellular proliferation and apoptosis of monocytes were assessed using cell counting kit‑8 assay and flow cytometry, respectively. miR‑211 was revealed to be targeted by HOTAIR and IL‑6R. The expression of IFN‑γ, IL‑6, IL‑17, TNF‑α, IL‑1β, IL‑6R and HOTAIR was significantly upregulated in the septic mice, whereas miR‑211 expression was downregulated. The overexpression of hox transcript antisense RNA (HOTAIR) and knockdown of miR‑211 were associated with an increased expression of IFN‑γ, IL‑6, IL‑17, TNF‑α, IL‑1β and IL‑6R in monocytes, while the overexpression of miR‑211 exhibited the opposite effect. HOTAIR overexpression and miR‑211 knockdown significantly inhibited cellular proliferation and promoted monocyte apoptosis, whereas the overexpression of miR‑211 exhibited the opposite effects in monocytes. Therefore, HOTAIR may promote the progression of sepsis by indirectly regulating the expression of IL‑6R via miR‑211.
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November-2019
Volume 18 Issue 5

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

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Spandidos Publications style
Chen J, Gu X, Zhou L, Wang S, Zhu L, Huang Y and Cao F: Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression. Exp Ther Med 18: 3959-3967, 2019
APA
Chen, J., Gu, X., Zhou, L., Wang, S., Zhu, L., Huang, Y., & Cao, F. (2019). Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression. Experimental and Therapeutic Medicine, 18, 3959-3967. https://doi.org/10.3892/etm.2019.8063
MLA
Chen, J., Gu, X., Zhou, L., Wang, S., Zhu, L., Huang, Y., Cao, F."Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression". Experimental and Therapeutic Medicine 18.5 (2019): 3959-3967.
Chicago
Chen, J., Gu, X., Zhou, L., Wang, S., Zhu, L., Huang, Y., Cao, F."Long non‑coding RNA‑HOTAIR promotes the progression of sepsis by acting as a sponge of miR‑211 to induce IL‑6R expression". Experimental and Therapeutic Medicine 18, no. 5 (2019): 3959-3967. https://doi.org/10.3892/etm.2019.8063