Co-inhibition of CD73 and ADORA2B Improves Long-Term Cigarette Smoke Induced Lung Injury.

ABSTRACT: Adenosine (ADO) involvement in lung injury depends on the activation of its receptors. The ADO A_2A receptor (ADORA2A) and A_2B receptor (ADORA2B) are best described to have both tissue-protective and tissue-destructive processes. However, no approach has been effective in delineating the mechanism(s) involved with ADO shifting from its tissue-protective to tissue-destructive properties in chronic airway injury. Using cigarette smoke (CS) as our model of injury, we chronically exposed Nuli-1 cells to 5% CS extract (CSE) for 3 years establishing a long-term CSE exposure model (LTC). We found significant morphological changes, decreased proliferation, and migration resulting in impaired airway wound closure in LTC. Further investigations showed that long-term CSE exposure

SUBMITTER: Tian Z 

PROVIDER: S-EPMC7876334 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature