Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway |
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| Authors: | Rui Xu Qi Li Xiang-Dong Zhou Juliy M Perelman Victor P Kolosov |
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| Affiliation: | 1.Department of Respiratory Medicine, the Second Affiliated Hospital, Chongqing University of Medical Science, Chongqing 400010, China; E-Mails: (R.X.); (Q.L.);2.Far Eastern Scientific Center of Physiology and Pathology of Respiration, Russian Academy of Medical Sciences, Blagoveschensk 675000, Russia; E-Mails: (J.M.P.); (V.P.K.) |
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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. |
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| Keywords: | oxidative stress tight junctions TRPM2 PLCγ 1 PKCα |
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