期刊
FASEB JOURNAL
卷 24, 期 1, 页码 70-80出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.09-140772
关键词
neutrophil; macrophage; emphysema; pulmonary fibrosis
资金
- U. S. National Institutes of Health [AI-43572, HL-70952, HL-095403]
- National Center for Research Resources [TL1RR024147]
- NATIONAL CENTER FOR RESEARCH RESOURCES [TL1RR024147] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R03HL095403, R01HL070952] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI043572] Funding Source: NIH RePORTER
Chronic obstructive pulmonary disease (COPD) is a major health concern. Adenosine, a signaling molecule generated in response to cell stress, contributes to the pathogenesis of COPD. An established model of adenosine-mediated lung injury is the adenosine deaminase-deficient (Ada(-/-)) mouse. Osteopontin (OPN) is a chemokine that is produced following injury and is implicated in a variety of human pathologies, but its expression and role in the pathogenesis of COPD have not been examined. To investigate the role of OPN in a model of COPD, Ada(-/-) double-knockout mice were generated, and inflammation and air-space enlargement endpoints were examined. Results demonstrate that Ada(-/-) mice exhibit OPN-dependent neutrophilia, alveolar air-space enlargement, and increases in mediators of air-space enlargement. Furthermore, we demonstrate that patients with COPD have increased OPN expression within distal airways in association with clinical airway obstruction. These results suggest that OPN represents a novel biomarker and therapeutic target for patients with COPD.-Schneider, D. J., Lindsay, J. C., Zhou, Y., Molina, J. G., Blackburn, M. R. Adenosine and osteopontin contribute to the development of chronic obstructive pulmonary disease. FASEB J. 24, 70-80 ( 2010). www.fasebj.org
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