TRPC6-dependent Ca²⁺ signaling mediates airway inflammation in response to oxidative stress via ERK pathway.

ABSTRACT: Ozone (O₃) plays an extremely important role in airway inflammation by generating reactive oxygen species (ROS) including hydrogen peroxide, then promoting redox actions and causing oxidative stress. Evidences indicate that TRPC6 (canonical transient receptor potential channel 6) is a redox-regulated Ca²⁺ permeable nonselective cation channel, but its role in the setting of oxidative stress-related airway inflammation remains unknown. Here, we found that both TRPC6^-/- mice and mice pretreated with SAR7334, a potent TRPC6 inhibitor, were protected from O₃-induced airway inflammatory responses. In vitro, both knockdown of TRPC6 expression with shRNA and TRPC6 blockage markedly attenuated the release of cytokines IL-6 and IL-8 induced by O₃

SUBMITTER: Chen Q 

PROVIDER: S-EPMC7058000 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature