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Downregulation of lung mitochondrial prohibitin in COPD
Authors:Soulitzis Nikolaos  Neofytou Eirini  Psarrou Maria  Anagnostis Aristotelis  Tavernarakis Nektarios  Siafakas Nikolaos  Tzortzaki Eleni G
Affiliation:Laboratory of Molecular and Cellular Pulmonology, Medical School, University of Crete, Heraklion, Greece.
Abstract:Prohibitins (PHB1 and PHB2) are versatile proteins located at the inner mitochondrial membrane, maintaining normal mitochondrial function and morphology. They interact with the NADH dehydrogenase protein complex, which is essential for oxidoreductase activity within cells. However, their expression in lung epithelium, especially in smokers and patients with inflammatory lung diseases associated with increased oxidative stress, such as COPD, is unknown. Lung tissue specimens from 45 male subjects were studied: 20 COPD patients [age: 65.7?±?5.8 years, smoking: 84.6?±?33.6 pack-years, FEV(1) (%pred.): 58.7?±?14.6, FEV(1)/FVC (%): 63.8?±?9.4], 15 non-COPD smokers [age: 59.0?±?12.1 years, smoking: 52.5?±?20.8 pack-years, FEV(1) (%pred.): 85.5?±?14.2, FEV(1)/FVC (%): 78.5?±?4.7] and 10 non-smokers. Quantitative real-time PCR experiments were carried out for PHB1 and PHB2, using β-actin as internal control. Non-COPD smokers exhibited lower PHB1 mRNA levels when compared to non-smokers (0.55?±?0.06 vs. 0.90?±?0.06, P?=?0.043), while PHB1 expression was even further decreased in COPD patients (0.32?±?0.02), a statistically significant finding vs. both non-COPD smokers (P?=?0.040) and non-smokers (P?
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