Journal
PLOS ONE
Volume 9, Issue 4, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0095600
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Funding
- Alpha-1 Foundation
- CHEST Foundation Clinical Research Award
- Michael Smith Foundation for Health Research Senior Scholarship award
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Oxidative stress is involved in the pathogenesis of airway obstruction in alpha(1)-antitrypsin deficient patients. This may result in a shortening of telomere length, resulting in cellular senescence. To test whether telomere length differs in alpha(1)-antitrypsin deficient patients compared with controls, we measured telomere length in DNA from peripheral blood cells of 217 alpha(1)-antitrypsin deficient patients and 217 control COPD patients. We also tested for differences in telomere length between DNA from blood and DNA from lung tissue in a subset of 51 controls. We found that telomere length in the blood was significantly longer in alpha(1)-antitrypsin deficient COPD patients compared with control COPD patients (p = 1x10(-29)). Telomere length was not related to lung function in alpha(1)-antitrypsin deficient patients (p = 0.3122) or in COPD controls (p = 0.1430). Although mean telomere length was significantly shorter in the blood when compared with the lungs (p = 0.0078), telomere length was correlated between the two tissue types (p = 0.0122). Our results indicate that telomere length is better preserved in alpha(1)-antitrypsin deficient COPD patients than in non-deficient patients. In addition, measurement of telomere length in the blood may be a suitable surrogate for measurement in the lung.
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