%0 Journal Article %A Reddy, Narsa M. %A Vegiraju, Suryanaraya %A Irving, Ashley %A Paun, Bogdan C. %A Luzina, Irina G. %A Atamas, Sergei P. %A Biswal, Shyam %A Ana, Navas-Acien %A Mitzner, Wayne %A Reddy, Sekhar P. %D 2012 %T Targeted Deletion of Jun/AP-1 in Alveolar Epithelial Cells Causes Progressive Emphysema and Worsens Cigarette Smoke-Induced Lung Inflammation %U https://indigo.uic.edu/articles/journal_contribution/Targeted_Deletion_of_Jun_AP-1_in_Alveolar_Epithelial_Cells_Causes_Progressive_Emphysema_and_Worsens_Cigarette_Smoke-Induced_Lung_Inflammation/10760009 %2 https://indigo.uic.edu/ndownloader/files/19271882 %K untagged %X The c-Jun/AP-1 transcriptional factor is known to regulate cell proliferation, apoptosis, and inflammatory responses; however its role in lung pathogenesis is largely unknown. Here we report that the declined expression levels of c-Jun mRNA and protein in the lung tissues of advanced chronic obstructive pulmonary disease (COPD) patients, and that genetic deletion of c-Jun specifically in alveolar epithelial cells causes progressive emphysema with lung inflammation and alveolar air space enlargement, which are cardinal features of emphysema. Although mice lacking c-Jun specifically in lung alveolar epithelial cells appear normal at 6 weeks of age, when exposed to chronic cigarette smoke, c-Jun mutant mice display more lung inflammation with perivascular and peribronchiolar infiltrates. These results demonstrate that the c-Jun/AP-1 pathway is critical for maintaining lung alveolar cell homeostasis and that loss of its expression can contribute to lung inflammation and progressive emphysema. %I University of Illinois at Chicago