Deregulation of apoptosis mediators' p53 and bcl2 in lung tissue of COPD patients

• Main Authors: Pentilas Nikolaos, Soulitzis Nikolaos, Psarrou Maria, Vlachaki Eleni, Neofytou Eirini, Koutsopoulos Anastasios V, Siganaki Marianna, Schiza Sophia, Siafakas Nikolaos M, Tzortzaki Eleni G
• Format: Article
• Language: English
• Published: BMC 2010-04-01
• Series: Respiratory Research
• Online Access: http://respiratory-research.com/content/11/1/46

<p>Abstract</p> <p>Abnormal apoptotic events in chronic obstructive pulmonary disease (COPD) subvert cellular homeostasis and may play a primary role in its pathogenesis. However, studies in human subjects are limited.</p> <p>p53 and bcl2 protein expression was measured by western blot on lung tissue specimens from 43 subjects (23 COPD smokers and 20 non-COPD smokers), using beta-actin as internal control. Additionally, p53 and bcl2 expression patterns were evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded lung tissue sections from the same individuals.</p> <p>Western blot analysis showed statistically significant increased p53 protein levels in COPD smokers in comparison with non-COPD smokers (p = 0.038), while bcl2 protein levels were not statistically different between the two groups. Lung immunohistochemistry showed increased ratio of positive p53-stained type II pneumocytes/total type II pneumocytes in COPD smokers compared to non-COPD smokers (p = 0.01), whereas the p53 staining ratio in alveolar macrophages and in lymphocyte-like cells did not differ statistically between the two groups. On the other hand, bcl2 expression did not differ between the two groups in all three cell types.</p> <p>The increased expression of pro-apoptotic p53 in type II pneumocytes of COPD patients not counterbalanced by the anti-apoptotic bcl2 could reflect increased apoptosis in the alveolar epithelium of COPD patients. Our results confirm previous experiments and support the hypothesis of a disturbance in the balance between the pro- and anti-apoptotic mediators in COPD.</p>