Open AccessLonger Telomere Length in COPD Patients with α1-Antitrypsin Deficiency Independent of Lung Function
Author(s) -
Aabida Saferali,
Jee Lee,
Don D. Sin,
Farshid N. Rouhani,
Mark Brantly,
Andrew J. Sandford
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0095600
Subject(s) - telomere , copd , senescence , lung , pathogenesis , telomerase , medicine , pulmonary function testing , oxidative stress , immunology , pathology , gastroenterology , biology , dna , genetics , gene
Oxidative stress is involved in the pathogenesis of airway obstruction in α 1 -antitrypsin deficient patients. This may result in a shortening of telomere length, resulting in cellular senescence. To test whether telomere length differs in α 1 -antitrypsin deficient patients compared with controls, we measured telomere length in DNA from peripheral blood cells of 217 α 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 α 1 -antitrypsin deficient COPD patients compared with control COPD patients (p = 1×10 −29 ). Telomere length was not related to lung function in α 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 α 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.