RT Journal Article
SR Electronic
T1 Expression of prohibitin 1 mitochondrial protein in non-COPD and COPD smokers
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 4720
VO 38
IS Suppl 55
A1 Nikolaos Soulitzis
A1 Eirini Neofytou
A1 Maria Psarrou
A1 Sotiris Menikou
A1 Nikolaos Siafakas
A1 Eleni Tzortzaki
YR 2011
UL http://erj.ersjournals.com/content/38/Suppl_55/4720.abstract
AB Introduction: Prohibitin 1 (PHB1) is a versatile protein that is located in the inner mitochondrial membrane, maintaining normal mitochondrial function and morphology. Prohibitin interacts with NADH dehydrogenase, a protein complex essential for the oxidoreductase activity within cells. However, its expression in lung epithelium, especially in patients with inflammatory lung diseases associated with increased oxidative stress, such as COPD, is unknown.Aim: To study PHB1 expression in lung tissue of non-smokers, non-COPD smokers and COPD patients.Methodology: Lung tissue specimens from 30 male subjects were studied: 15 COPD patients [age: 65.9±6.2 years, smoking: 88.9±35.2 pack-years, FEV1 (% pred): 58.4±16.4, FEV1/FVC (%): 66.2±8.6], 10 non-COPD smokers [age: 57.0±11.7 years, smoking: 67.1±39.9 pack-years, FEV1 (% pred): 84.0±15.9, FEV1/FVC (%): 80.0±3.8] and 5 non-smokers. Quantitative Real-Time PCR and Western Blot experiments were carried out for PHB1, using beta-actin as internal control.Results: Non-COPD smokers exhibited lower prohibitin levels when compared to non-smokers (0.55±0.06 vs. 0.90±0.06, p=0.011), while PHB1 mRNA levels were even further decreased in COPD patients (0.32±0.02), a finding statistically significant vs. both non-COPD smokers (p=0.012) and non-smokers (p=0.009). Western blot analysis verified the above results (non-smokers: 1.77±0.10; non-COPD smokers: 0.97±0.08; COPD patients: 0.62±0.09, p=0.028).Conclusion: The significantly downregulated prohibitin levels in non-COPD and COPD smokers in comparison with non-smokers possibly reflects a distorted mitochondrial function, resulting in decreased anti-oxidant activity, especially in the mitochondria of COPD patients.