Original Research |

Decreased serum sirtuin-1 in chronic obstructive pulmonary disease OPEN ACCESS

Satoru Yanagisawa, Ph.D.; Andriana I. Papaioannou, Ph.D.; Anastasia Papaporfyriou, Ph.D.; Jonathan Baker, Ph.D.; Chaitanya Vuppusetty, M.Sc.; Stelios Loukides, Ph.D.; Peter J. Barnes, FRS; Kazuhiro Ito, Ph.D.
Author and Funding Information

Author’s contributions

SY conducted assay, carried out the data analysis and drafted the manuscript. JB conducted assay with primary epithelial cells. AIP, AP, CV, SL were involved in sample preparation and participated in the design of the original study. PB participated in the design of the study, and contributed substantially to preparation of manuscript. KI contributed to the data analysis, design of the study and the manuscript preparation.

All sources of support:

This project was supported by the Wellcome Trust Programme Grant 093080/Z/10/Z. SY is a recipient of a Banyu Life Science Foundation International fellowship. CV and JB are recipients of the Wellcome Trust grant.

1Airway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom

2Third Respiratory Medicine Department, Sismanogleion General Hospital, Athens Greece

3First respiratory Medicine Department, University of Athens, Sotiria Hospital, Athens Greece

4Division of Respiratory Diseases I, National and Kapodistrian University of Athens, Athens Greece

Correspondence should be addressed to: Kazuhiro Ito Airway Disease Section, National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse St, London SW3 6LY, UK.

Copyright 2017, . All Rights Reserved.

Chest. 2017. doi:10.1016/j.chest.2017.05.004
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Background  The protein deacetylase sirtuin-1 (SIRT1) is an anti-aging molecule that is decreased in the lung from patients with chronic obstructive pulmonary disease (COPD). Recently, SIRT1 was reported to be detectable in serum, but serum SIRT1 levels have not yet been reported in patients with COPD.

Methods  Serum SIRT1 was measured by Western blotting, and relative ratio of band density in samples against that of a positive control were calculated.

Results  Several molecular sizes of SIRT1, including 120kDa (actual size) and fragments (102, 75kDa) were quantified by Western blotting. Among them, only the 120kDa serum SIRT1 (s120S) was significantly decreased in the patients with COPD compared to the control subjects without COPD (s120S ratio in healthy: 0.90±0.34, vs COPD: 0.68±0.24; p=0.014), and was positively correlated with airway obstruction (FEV1/ FVC; r=0.31; p=0.020) and its severity measured by FEV1 % predicted (r=0.29; p=0.029). Serum s120S also showed a positive correlation with body mass index (BMI; r=0.36; p=0.0077) and diffusing capacity of the lung per unit volume (KCO%; r=0.32; p=0.025). It was also significantly decreased with increasing severity of lung emphysema (r=-0.40, p=0.027) and with a clinical history of frequent COPD exacerbations (infrequent: 0.76±0.20 vs frequent: 0.56±0.26; p=0.027). SIRT1 was not detected in supernatant of A549 and primary epithelial cells in normal culture condition.

Conclusions  Serum SIRT1 (s120S) was decreased in the patients with COPD, potentially as reflected by the reduced SIRT1 within cells as a result of oxidative stress, and might be a potential biomarkers for certain disease characteristics of COPD.

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