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Int. J. Mol. Sci. 2013, 14(5), 9475-9486;

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

Department of Respiratory Medicine, the Second Affiliated Hospital, Chongqing University of Medical Science, Chongqing 400010, China
Far Eastern Scientific Center of Physiology and Pathology of Respiration, Russian Academy of Medical Sciences, Blagoveschensk 675000, Russia
Author to whom correspondence should be addressed.
Received: 24 January 2013 / Revised: 18 March 2013 / Accepted: 16 April 2013 / Published: 29 April 2013
(This article belongs to the Special Issue Oxidative Stress and Ageing)
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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. View Full-Text
Keywords: oxidative stress; tight junctions; TRPM2; PLCγ1; PKCα oxidative stress; tight junctions; TRPM2; PLCγ1; PKCα
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Xu, R.; Li, Q.; Zhou, X.-D.; Perelman, J.M.; Kolosov, V.P. Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway. Int. J. Mol. Sci. 2013, 14, 9475-9486.

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