Role of chronic exsposure to cigarette smoke on endoglin/CD105 expression in airway epithelium.

Dysregulation of airway epithelial cell function related to cigarette smoke exposure plays animportant role in the pathophysiology of COPD and is associated to tissue damage and diseaseseverity. CD105 is a component of the receptor complex of TGF-β, a pleiotropic cytokine involvedin cellular proliferation, differentiation and migration. CD105 regulates the expression of differentcomponents of the extracellular matrix suggesting a role of CD105 in cellular transmigration andremodeling processes.The aim of the present study was to investigate the expression of endoglin/CD105 in airwayepithelium of COPD patients and its involvement in tissue remodeling and progression of COPD.We evaluated the immunoreactivity for CD105 expression in bronchial biopsies isolated fromCOPD patients and healthy controls (HC). The analysis of metaplastic epithelium was performed inbronchial biopsies by Image Analysis software (Leica Quantimet system). Finally, we investigatedthe expression of CD105 protein receptor in human bronchial epithelial cells (16HBE cells)exposed to 5% Cigarette Smoke Extract (CSE) for 12 days by western blot.We found that the CD105 immunoreactivity was significantly higher in bronchial epithelium ofCOPD than HC. Morphometric analysis of bioptic samples of COPD showed an increase of theimmunoreactivity for CD105 in the area of metaplastic than in not metaplastic epithelium. Longterm exposure to CSE significantly up-regulated CD105 expression in 16HBE.Chronic inflammation due to cigarette smoke might play a critic role on the alteration of CD105protein expression in COPD, promoting tissue remodeling, angiogenesis and dysregulation ofphysiological reparative mechanisms, leading to squamous metaplasia.