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

International Journal of Molecular Sciences

Rui Xu²  Qi Li²  Xiang-Dong Zhou²  Juliy M. Perelman¹ 

[1] Far Eastern Scientific Center of Physiology and Pathology of Respiration, Russian Academy of Medical Sciences, Blagoveschensk 675000, Russia; E-Mails:;Department of Respiratory Medicine, the Second Affiliated Hospital, Chongqing University of Medical Science, Chongqing 400010, China; E-Mails:

关键词: oxidative stress;    tight junctions;    TRPM2;    PLCγ1;    PKCα;   

DOI  :  10.3390/ijms14059475

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland