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DDX3X deficiency alleviates LPS-induced H9c2 cardiomyocytes pyroptosis by suppressing activation of NLRP3 inflammasome
Increasing evidence suggest that NOD-like receptor protein 3 (NLRP3) inflammasome-mediated pyroptosis may be the underlying pathological mechanism of sepsis-induced cardiomyopathy. DDX3X, an ATP-dependent RNA helicase, plays a vital role in the formation of the NLRP3 inflammasome by directly interac...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8506920/ https://www.ncbi.nlm.nih.gov/pubmed/34650637 http://dx.doi.org/10.3892/etm.2021.10825 |
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author | Feng, Dandan Guo, Liang Liu, Jing Song, Yunxuan Ma, Xiuyuan Hu, Haiyang Liu, Ju Hao, Enkui |
author_facet | Feng, Dandan Guo, Liang Liu, Jing Song, Yunxuan Ma, Xiuyuan Hu, Haiyang Liu, Ju Hao, Enkui |
author_sort | Feng, Dandan |
collection | PubMed |
description | Increasing evidence suggest that NOD-like receptor protein 3 (NLRP3) inflammasome-mediated pyroptosis may be the underlying pathological mechanism of sepsis-induced cardiomyopathy. DDX3X, an ATP-dependent RNA helicase, plays a vital role in the formation of the NLRP3 inflammasome by directly interacting with cytoplasmic NLRP3. However, whether DDX3X has a direct impact on lipopolysaccharide (LPS)-induced cardiomyocyte injury by regulating NLRP3 inflammasome assembly remains unclear. The present study aimed to investigate the role of DDX3X in the activation of the NLRP3 inflammasome and determine the molecular mechanism of DDX3X action in LPS-induced pyroptosis in H9c2 cardiomyocytes. H9c2 cardiomyocytes were treated with LPS to simulate sepsis in vitro. The results demonstrated that LPS stimulation upregulated DDX3X expression in H9c2 cardiomyocytes. Furthermore, Ddx3x knockdown significantly attenuated pyroptosis and cell injury in LPS-treated H9c2 cells by suppressing NLRP3 inflammasome activation. Taken together, these results suggest that DDX3X is involved in LPS-induced cardiomyocyte pyroptosis, and DDX3X deficiency mitigates cardiomyocyte damage induced by LPS treatment. |
format | Online Article Text |
id | pubmed-8506920 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-85069202021-10-13 DDX3X deficiency alleviates LPS-induced H9c2 cardiomyocytes pyroptosis by suppressing activation of NLRP3 inflammasome Feng, Dandan Guo, Liang Liu, Jing Song, Yunxuan Ma, Xiuyuan Hu, Haiyang Liu, Ju Hao, Enkui Exp Ther Med Articles Increasing evidence suggest that NOD-like receptor protein 3 (NLRP3) inflammasome-mediated pyroptosis may be the underlying pathological mechanism of sepsis-induced cardiomyopathy. DDX3X, an ATP-dependent RNA helicase, plays a vital role in the formation of the NLRP3 inflammasome by directly interacting with cytoplasmic NLRP3. However, whether DDX3X has a direct impact on lipopolysaccharide (LPS)-induced cardiomyocyte injury by regulating NLRP3 inflammasome assembly remains unclear. The present study aimed to investigate the role of DDX3X in the activation of the NLRP3 inflammasome and determine the molecular mechanism of DDX3X action in LPS-induced pyroptosis in H9c2 cardiomyocytes. H9c2 cardiomyocytes were treated with LPS to simulate sepsis in vitro. The results demonstrated that LPS stimulation upregulated DDX3X expression in H9c2 cardiomyocytes. Furthermore, Ddx3x knockdown significantly attenuated pyroptosis and cell injury in LPS-treated H9c2 cells by suppressing NLRP3 inflammasome activation. Taken together, these results suggest that DDX3X is involved in LPS-induced cardiomyocyte pyroptosis, and DDX3X deficiency mitigates cardiomyocyte damage induced by LPS treatment. D.A. Spandidos 2021-12 2021-09-30 /pmc/articles/PMC8506920/ /pubmed/34650637 http://dx.doi.org/10.3892/etm.2021.10825 Text en Copyright: © Feng et al. https://creativecommons.org/licenses/by-nc-nd/4.0/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 Feng, Dandan Guo, Liang Liu, Jing Song, Yunxuan Ma, Xiuyuan Hu, Haiyang Liu, Ju Hao, Enkui DDX3X deficiency alleviates LPS-induced H9c2 cardiomyocytes pyroptosis by suppressing activation of NLRP3 inflammasome |
title | DDX3X deficiency alleviates LPS-induced H9c2 cardiomyocytes pyroptosis by suppressing activation of NLRP3 inflammasome |
title_full | DDX3X deficiency alleviates LPS-induced H9c2 cardiomyocytes pyroptosis by suppressing activation of NLRP3 inflammasome |
title_fullStr | DDX3X deficiency alleviates LPS-induced H9c2 cardiomyocytes pyroptosis by suppressing activation of NLRP3 inflammasome |
title_full_unstemmed | DDX3X deficiency alleviates LPS-induced H9c2 cardiomyocytes pyroptosis by suppressing activation of NLRP3 inflammasome |
title_short | DDX3X deficiency alleviates LPS-induced H9c2 cardiomyocytes pyroptosis by suppressing activation of NLRP3 inflammasome |
title_sort | ddx3x deficiency alleviates lps-induced h9c2 cardiomyocytes pyroptosis by suppressing activation of nlrp3 inflammasome |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8506920/ https://www.ncbi.nlm.nih.gov/pubmed/34650637 http://dx.doi.org/10.3892/etm.2021.10825 |
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