Angiogenesis of bronchial vessels and apoptosis of lung structural cells are important mechanisms involved in the development of COPD. Endoglin (CD105), a proliferation-associated protein abundantly present on angiogenic endothelial cells, is strongly expressed in lung carcinoma but its expression in COPD has never been evaluated. Similarly, the airway epithelial expression of Bcl-xL and Fas (CD95), two molecules regulating the apoptosis pathway, has been scarcely investigated in COPD. Our purpose was to verify whether in symptomatic smokers the presence of a contralateral non small cell lung cancer (NSCLC) can influence the degree of bronchial angiogenesis and can be associated to cell cycle modifications occurring in distant apparently normal mucosa. Bronchial biopsies were obtained from two groups of symptomatic smokers: 12 with a contralateral NSCLC and 13 without NSCLC. Vessels in the lamina propria were identified by using mAbs against the pan-endothelial marker CD 31 and the more specific CD 105. Bcl-xL and CD95 expression was evaluated using the respective mAbs. No significant difference in the expression of CD105 by bronchial vessels was detected between the two groups. However, the number of CD105+ vessels was increased in the lamina propria below metaplastic/displastic squamous bronchial epithelium in smokers with NSCLC. Furthermore, preliminar results show a lower expression of Fas and a higher expression of Bcl-xL in the metaplastic/displastic bronchial epithelium of smokers with NSCLC. These results suggest that cell cycle modifications and increased bronchial angiogenesis can be associated to more aggressive preneoplastic lesions.

Angiogenetic and apoptotic process in the airways of symptomatic smokers with and without a contralateral non small cell lung cancer

VATRELLA, Alessandro
2009

Abstract

Angiogenesis of bronchial vessels and apoptosis of lung structural cells are important mechanisms involved in the development of COPD. Endoglin (CD105), a proliferation-associated protein abundantly present on angiogenic endothelial cells, is strongly expressed in lung carcinoma but its expression in COPD has never been evaluated. Similarly, the airway epithelial expression of Bcl-xL and Fas (CD95), two molecules regulating the apoptosis pathway, has been scarcely investigated in COPD. Our purpose was to verify whether in symptomatic smokers the presence of a contralateral non small cell lung cancer (NSCLC) can influence the degree of bronchial angiogenesis and can be associated to cell cycle modifications occurring in distant apparently normal mucosa. Bronchial biopsies were obtained from two groups of symptomatic smokers: 12 with a contralateral NSCLC and 13 without NSCLC. Vessels in the lamina propria were identified by using mAbs against the pan-endothelial marker CD 31 and the more specific CD 105. Bcl-xL and CD95 expression was evaluated using the respective mAbs. No significant difference in the expression of CD105 by bronchial vessels was detected between the two groups. However, the number of CD105+ vessels was increased in the lamina propria below metaplastic/displastic squamous bronchial epithelium in smokers with NSCLC. Furthermore, preliminar results show a lower expression of Fas and a higher expression of Bcl-xL in the metaplastic/displastic bronchial epithelium of smokers with NSCLC. These results suggest that cell cycle modifications and increased bronchial angiogenesis can be associated to more aggressive preneoplastic lesions.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11386/3877595
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