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Int. J. Mol. Sci. 2013, 14(5), 9475-9486; doi:10.3390/ijms14059475
Article

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

1
, 1
, 1,* , 2
 and 2
Received: 24 January 2013; in revised form: 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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Abstract: 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.
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 which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

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.

AMA Style

Xu R, Li Q, Zhou X-D, Perelman JM, Kolosov VP. Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway. International Journal of Molecular Sciences. 2013; 14(5):9475-9486.

Chicago/Turabian Style

Xu, Rui; Li, Qi; Zhou, Xiang-Dong; Perelman, Juliy M.; Kolosov, Victor P. 2013. "Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway." Int. J. Mol. Sci. 14, no. 5: 9475-9486.


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