PT  - JOURNAL ARTICLE
AU  - Nikolaos Soulitzis
AU  - Eirini Neofytou
AU  - Maria Psarrou
AU  - Sotiris Menikou
AU  - Nikolaos Siafakas
AU  - Eleni Tzortzaki
TI  - Expression of prohibitin 1 mitochondrial protein in non-COPD and COPD smokers
DP  - 2011 Sep 01
TA  - European Respiratory Journal
PG  - 4720
VI  - 38
IP  - Suppl 55
4099  - http://erj.ersjournals.com/content/38/Suppl_55/4720.short
4100  - http://erj.ersjournals.com/content/38/Suppl_55/4720.full
SO  - Eur Respir J2011 Sep 01; 38
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.