Longer telomere length in COPD patients with α1-antitrypsin deficiency independent of lung function

PLoS One. 2014 Apr 24;9(4):e95600. doi: 10.1371/journal.pone.0095600. eCollection 2014.

Abstract

Oxidative stress is involved in the pathogenesis of airway obstruction in α1-antitrypsin deficient patients. This may result in a shortening of telomere length, resulting in cellular senescence. To test whether telomere length differs in α1-antitrypsin deficient patients compared with controls, we measured telomere length in DNA from peripheral blood cells of 217 α1-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 α1-antitrypsin deficient COPD patients compared with control COPD patients (p = 1×10(-29)). Telomere length was not related to lung function in α1-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 α1-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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Case-Control Studies
  • Female
  • Forced Expiratory Volume
  • Humans
  • Lung / pathology
  • Lung / physiopathology
  • Male
  • Middle Aged
  • Organ Specificity
  • Pulmonary Disease, Chronic Obstructive / genetics*
  • Pulmonary Disease, Chronic Obstructive / physiopathology
  • Telomere / genetics*
  • Telomere Homeostasis
  • alpha 1-Antitrypsin Deficiency / genetics*
  • alpha 1-Antitrypsin Deficiency / physiopathology

Grants and funding

This study was funded by an Alpha-1 Foundation and CHEST Foundation Clinical Research Award. AJS was the recipient of a Michael Smith Foundation for Health Research Senior Scholarship award. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.