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

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 remai...

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Autores principales: Liu, Lingling, Liu, Fengtao, Sun, Zhilu, Peng, Zhengliang, You, Ting, Yu, Ziying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444425/
https://www.ncbi.nlm.nih.gov/pubmed/32855700
http://dx.doi.org/10.3892/etm.2020.9079
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author Liu, Lingling
Liu, Fengtao
Sun, Zhilu
Peng, Zhengliang
You, Ting
Yu, Ziying
author_facet Liu, Lingling
Liu, Fengtao
Sun, Zhilu
Peng, Zhengliang
You, Ting
Yu, Ziying
author_sort Liu, Lingling
collection PubMed
description 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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spelling pubmed-74444252020-08-26 LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p Liu, Lingling Liu, Fengtao Sun, Zhilu Peng, Zhengliang You, Ting Yu, Ziying Exp Ther Med Articles 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. D.A. Spandidos 2020-10 2020-07-29 /pmc/articles/PMC7444425/ /pubmed/32855700 http://dx.doi.org/10.3892/etm.2020.9079 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Liu, Lingling
Liu, Fengtao
Sun, Zhilu
Peng, Zhengliang
You, Ting
Yu, Ziying
LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p
title LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p
title_full LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p
title_fullStr LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p
title_full_unstemmed LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p
title_short LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p
title_sort lncrna neat1 promotes apoptosis and inflammation in lps-induced sepsis models by targeting mir-590-3p
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7444425/
https://www.ncbi.nlm.nih.gov/pubmed/32855700
http://dx.doi.org/10.3892/etm.2020.9079
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