TY - JOUR T1 - Beclin1 circulating levels and accelerated ageing markers in COPD JF - European Respiratory Journal JO - Eur Respir J DO - 10.1183/1393003.congress-2017.PA1018 VL - 50 IS - suppl 61 SP - PA1018 AU - Frédéric Schlemmer AU - Laurent Boyer AU - Thibaud Soumagne AU - Audrey Ridoux AU - Lucie Bizard AU - Elisabeth Marcos AU - Bruno Housset AU - Christos Chouaid AU - Bernard Maitre AU - Sophie Lanone AU - Serge Adnot AU - Etienne Audureau AU - Jorge Boczkowski Y1 - 2017/09/01 UR - http://erj.ersjournals.com/content/50/suppl_61/PA1018.abstract N2 - Background: Cigarette smoke exposure can trigger the activation of several processes such as oxidative stress, cellular senescence and autophagy. Preliminary data suggest that an acquired defect in autophagic processes may occur in the course of COPD.Aims and objectives: Assuming that circulating Beclin1 levels may reflect the efficiency of autophagy process, we hypothesized that decreased circulating Beclin1 levels might be used to detect autophagy deficiency. Given that cellular senescence is involved in COPD pathophysiology and that autophagy defect may be a trigger of this process, we tested whether Beclin1 levels are linked to the reduction of telomere length, a hallmark of senescence.Methods: Quantitative evaluation of Beclin1 protein level (ELISA Kit; E98557Hu, Uscn Life Science Inc., China) were performed in the sera of 280 subjects (non-smokers n=95, smokers n=93, COPD n=92) already well phenotyped with a special focus on ageing-related markers (Boyer, L. et al. PLoS One 2015 Mar 18;10(3)).Results: Beclin1 protein level was correlated to age (R=-0.13; p Corr Pearson=0.027), FEV1 (R=0.12; p=0.039), telomere length (R=0.17; p=0.005) and appendicular skeletal muscle mass index (R=0.21; p=0.001). After adjustment for age, a statistically significant negative trend was found in serum Beclin1 protein level of non-smokers, smokers and COPD patients (2.31±0.23, 1.66±0.23 and 1.52±0.24 ng/ml, respectively; p=0.036).Conclusions: Serum Beclin1 levels are decreased in COPD patients and are correlated with FEV1 and markers of accelerated ageing. These results support the hypothesis of a potential link between defective autophagy, senescence and COPD pathogenesis. ER -