Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway

Oxidative stress has been implicated as an important contributing factor in the pathogenesis of several pulmonary inflammatory diseases. Previous studies have indicated a relationship between oxidative stress and the attenuation of epithelial tight junctions (TJs). In Human Bronchial Epithelial-16 c...

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Detalles Bibliográficos
Autores principales: Xu, Rui, Li, Qi, Zhou, Xiang-Dong, Perelman, Juliy M., Kolosov, Victor P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2013
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3676794/
https://www.ncbi.nlm.nih.gov/pubmed/23629676
http://dx.doi.org/10.3390/ijms14059475
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author Xu, Rui
Li, Qi
Zhou, Xiang-Dong
Perelman, Juliy M.
Kolosov, Victor P.
author_facet Xu, Rui
Li, Qi
Zhou, Xiang-Dong
Perelman, Juliy M.
Kolosov, Victor P.
author_sort Xu, Rui
collection PubMed
description Oxidative stress has been implicated as an important contributing factor in the pathogenesis of several pulmonary inflammatory diseases. Previous studies have indicated a relationship between oxidative stress and the attenuation of epithelial tight junctions (TJs). In Human Bronchial Epithelial-16 cells (16HBE), we demonstrated the degradation of zonula occludens-1 (ZO-1), and claudin-2 exhibited a great dependence on the activation of the transient receptor potential melastatin (TRPM) 2 channel, phospholipase Cγ1 (PLCγ1) and the protein kinase Cα (PKCα) signaling cascade.
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spelling pubmed-36767942013-07-02 Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway Xu, Rui Li, Qi Zhou, Xiang-Dong Perelman, Juliy M. Kolosov, Victor P. Int J Mol Sci Article Oxidative stress has been implicated as an important contributing factor in the pathogenesis of several pulmonary inflammatory diseases. Previous studies have indicated a relationship between oxidative stress and the attenuation of epithelial tight junctions (TJs). In Human Bronchial Epithelial-16 cells (16HBE), we demonstrated the degradation of zonula occludens-1 (ZO-1), and claudin-2 exhibited a great dependence on the activation of the transient receptor potential melastatin (TRPM) 2 channel, phospholipase Cγ1 (PLCγ1) and the protein kinase Cα (PKCα) signaling cascade. Molecular Diversity Preservation International (MDPI) 2013-04-29 /pmc/articles/PMC3676794/ /pubmed/23629676 http://dx.doi.org/10.3390/ijms14059475 Text en © 2013 by the authors; licensee MDPI, Basel, Switzerland http://creativecommons.org/licenses/by/3.0 This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Xu, Rui
Li, Qi
Zhou, Xiang-Dong
Perelman, Juliy M.
Kolosov, Victor P.
Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway
title Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway
title_full Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway
title_fullStr Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway
title_full_unstemmed Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway
title_short Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway
title_sort oxidative stress mediates the disruption of airway epithelial tight junctions through a trpm2-plcγ1-pkcα signaling pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3676794/
https://www.ncbi.nlm.nih.gov/pubmed/23629676
http://dx.doi.org/10.3390/ijms14059475
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