期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 180, 期 2, 页码 562-574出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2011.10.029
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资金
- National Institute of Environmental Health Sciences [ES007141]
- NIH [RO1-ES11863, RO1-HL66109, RO3-HL96933]
- Flight Attendant Medical Research Institute
- Acute Lung Injury-Specialized Centers of Clinically Oriented Research (ALI-SCCOR) [P50-HL073994]
- Chronic Obstructive Pulmonary Disease-Specialized Centers of Clinically Oriented Research (COPD-SCCOR) [P50-HL084945]
Chronic obstructive pulmonary disease appears to occur slowly and progressively over many years, with both genetic factors and environmental modifiers contributing to its pathogenesis. Although the c-Jun/activator protein 1 transcriptional factor regulates cell proliferation, apoptosis, and inflammatory responses, its role in lung pathogenesis is largely unknown. In this study, we report decreased expression levels of c-Jun mRNA and protein in the lung tissues of patients with advanced chronic obstructive pulmonary disease, and the 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 the age of 6 weeks, when exposed to long-term cigarette smoke, c-Jun mutant mice display more lung inflammation with perivascular and peribronchiolar infiltrates compared with controls. These results demonstrate that the c-Jun/activator protein 1 pathway is critical for maintaining lung alveolar cell homeostasis and that loss of its expression can contribute to lung inflammation and progressive emphysema. (Am J Pathol 2012, 180:562-574; DOI. 10.1016/j.ajpath.2011.10.029)
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