Dysregulation of airway epithelial cell function related to cigarette smoke exposure plays an
important role in the pathophysiology of COPD and is associated to tissue damage and disease
severity. CD105 is a component of the receptor complex of TGF-β, a pleiotropic cytokine involved
in cellular proliferation, differentiation and migration. CD105 regulates the expression of different
components of the extracellular matrix suggesting a role of CD105 in cellular transmigration and
remodeling processes.
The aim of the present study was to investigate the expression of endoglin/CD105 in airway
epithelium of COPD patients and its involvement in tissue remodeling and progression of COPD.
We evaluated the immunoreactivity for CD105 expression in bronchial biopsies isolated from
COPD patients and healthy controls (HC). The analysis of metaplastic epithelium was performed in
bronchial biopsies by Image Analysis software (Leica Quantimet system). Finally, we investigated
the 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 of
COPD than HC. Morphometric analysis of bioptic samples of COPD showed an increase of the
immunoreactivity for CD105 in the area of metaplastic than in not metaplastic epithelium. Long
term 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 CD105
protein expression in COPD, promoting tissue remodeling, angiogenesis and dysregulation of
physiological reparative mechanisms, leading to squamous metaplasia