Open Access

LncRNA NEAT1 promotes apoptosis and inflammation in LPS‑induced sepsis models by targeting miR‑590‑3p

  • Authors:
    • Lingling Liu
    • Fengtao Liu
    • Zhilu Sun
    • Zhengliang Peng
    • Ting You
    • Ziying Yu
  • View Affiliations

  • Published online on: July 29, 2020     https://doi.org/10.3892/etm.2020.9079
  • Pages: 3290-3300
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Sepsis is a complication of infection caused by disease or trauma. Increasing evidence have shown that long noncoding RNAs (lncRNAs) are involved in the regulation of sepsis. However, the mechanism of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in the regulation of sepsis progression remains to be elucidated. Lipopolysaccharide (LPS) was used to induce a sepsis cell model. The expression levels of NEAT1 and microRNA (miR)‑590‑3p were determined by reverse transcription‑quantitative PCR. Cell viability and apoptosis were detected using Cell Counting Kit‑8 (CCK‑8) assay and flow cytometry, respectively. Western blot analysis was performed to evaluate the levels of apoptosis‑ and NF‑κB signaling pathway‑related proteins. The concentration of inflammatory cytokines was determined using ELISA. In addition, dual‑luciferase reporter assay, RNA immunoprecipitation and biotin‑labeled RNA pull‑down assay were performed to verify the interaction between NEAT1 and miR‑590‑3p. The results showed that NEAT1 was highly expressed in patients with sepsis and LPS‑induced H9c2 cells. Knockdown of NEAT1 decreased LPS‑induced cell apoptosis and inflammation response in H9c2 cells. Meanwhile, miR‑590‑3p showed decreased expression in sepsis, and its overexpression could relieve LPS‑induced H9c2 cell damage. Further experiments revealed that NEAT1 could sponge miR‑590‑3p. Knockdown of miR‑590‑3p reversed the inhibitory effect of NEAT1 knockdown on LPS‑induced H9c2 cell damage. Additionally, the NEAT1/miR‑590‑3p axis could regulate the activity of the NF‑κB signaling pathway. To conclude, lncRNA NEAT1 accelerated apoptosis and inflammation in LPS‑stimulated H9c2 cells via sponging miR‑590‑3p. These findings may provide a new strategy for the treatment of sepsis.
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October-2020
Volume 20 Issue 4

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

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Spandidos Publications style
Liu L, Liu F, Sun Z, Peng Z, You T and Yu Z: LncRNA NEAT1 promotes apoptosis and inflammation in LPS‑induced sepsis models by targeting miR‑590‑3p. Exp Ther Med 20: 3290-3300, 2020
APA
Liu, L., Liu, F., Sun, Z., Peng, Z., You, T., & Yu, Z. (2020). LncRNA NEAT1 promotes apoptosis and inflammation in LPS‑induced sepsis models by targeting miR‑590‑3p. Experimental and Therapeutic Medicine, 20, 3290-3300. https://doi.org/10.3892/etm.2020.9079
MLA
Liu, L., Liu, F., Sun, Z., Peng, Z., You, T., Yu, Z."LncRNA NEAT1 promotes apoptosis and inflammation in LPS‑induced sepsis models by targeting miR‑590‑3p". Experimental and Therapeutic Medicine 20.4 (2020): 3290-3300.
Chicago
Liu, L., Liu, F., Sun, Z., Peng, Z., You, T., Yu, Z."LncRNA NEAT1 promotes apoptosis and inflammation in LPS‑induced sepsis models by targeting miR‑590‑3p". Experimental and Therapeutic Medicine 20, no. 4 (2020): 3290-3300. https://doi.org/10.3892/etm.2020.9079