Cigarette Smoke Impairs A_2A Adenosine Receptor Mediated Wound Repair through Up-regulation of Duox-1 Expression.

ABSTRACT: Cigarette smoke (CS) exposure and intrinsic factors such as the NADPH oxidases produce high levels of reactive oxygen species (ROS), ensuing inflammatory tissue injury. We previously demonstrated that CS-generated ROS, particularly hydrogen peroxide (H₂O₂), impaired adenosine stimulated wound repair. We hypothesized that CS exposure modulates expression of Dual oxidase 1 (Duox-1), a NADPH oxidases known to generate H₂O₂. To test this hypothesis, we used human bronchial epithelial cell line Nuli-1 and C57BL/6 mice. Cells were treated with 5% CS extract (CSE) for various periods of time, and mice were exposed to whole body CS for six weeks. Both CSE and CS treatment induced increased expression of Duox-1, and silencing of Doux-1 improved the rate o

SUBMITTER: Tian Z 

PROVIDER: S-EPMC5364501 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature