Oxidative Stress Mediates the Disruption of Airway Epithelial Tight Junctions through a TRPM2-PLCγ1-PKCα Signaling Pathway
Copyright policy )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 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.
- Far Eastern Scientific Centre of Physiology and Pathology of Respiration Russian Academy of Medical Sciences Russian Federation
- Chongqing Medical University China (People's Republic of)
- Department of Medical Sciences Russian Federation
- Russian Academy of Sciences Russian Federation
- Far Eastern Scientific Center of Physiology and Pathology of Respiration
tight junctions, Cell Membrane Permeability, Protein Kinase C-alpha, PLCγ1, Blotting, Western, TRPM Cation Channels, Bronchi, Article, Cell Line, Tight Junctions, Electric Impedance, oxidative stress, Humans, TRPM2, RNA, Small Interfering, Phospholipase C gamma, PKCα, Epithelial Cells, Hydrogen Peroxide, Oxidative Stress, Claudins, Zonula Occludens-1 Protein, Oxidation-Reduction, Signal Transduction
tight junctions, Cell Membrane Permeability, Protein Kinase C-alpha, PLCγ1, Blotting, Western, TRPM Cation Channels, Bronchi, Article, Cell Line, Tight Junctions, Electric Impedance, oxidative stress, Humans, TRPM2, RNA, Small Interfering, Phospholipase C gamma, PKCα, Epithelial Cells, Hydrogen Peroxide, Oxidative Stress, Claudins, Zonula Occludens-1 Protein, Oxidation-Reduction, Signal Transduction
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