Impaired non-homologous end joining in human primary alveolar type II cells in emphysema.

ABSTRACT: Emphysema is characterized by alveolar wall destruction induced mainly by cigarette smoke. Oxidative damage of DNA may contribute to the pathophysiology of this disease. We studied the impairment of the non-homologous end joining (NHEJ) repair pathway and DNA damage in alveolar type II (ATII) cells and emphysema development. We isolated primary ATII cells from control smokers, nonsmokers, and patients with emphysema to determine DNA damage and repair. We found higher reactive oxygen species generation and DNA damage in ATII cells obtained from individuals with this disease  in comparison with controls. We also observed low phosphorylation of H2AX, which activates DSBs repair signaling, in emphysema. Our results indicate the impairement  of NHEJ, as detected by low XLF expression. We also a

SUBMITTER: Kosmider B 

PROVIDER: S-EPMC6351635 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature