Pulmonary gene expression of tenascin-C and fibronectin in chronic obtructive pulmonary disease (COPD)

BACKGROUND COPD is characterized by pulmonary vascular remodeling and is associated with high prevalence of cardiovascular events regardless of other risk factors. Tenascin-C (TNC) and fibronectin (EDA-FN) are extracellular matrix proteins involved in cardiovascular pathology and in lung fibroproliferative diseases. Our principal aim was to elucidate whether this lung gene expression is different between COPD and smokers patients. METHODS Specimens of lung tissue from two groups, COPD and smokers without COPD, both who required surgery for lung cancer were studied. Clinical and spirometric data were collected. Gene expression was measured by quantitative polymerase chain reaction (Real time PCR) using comparative method (Ct) and RQ (fold change ratio) as a unit of measure. RESULTS Ten of the 28 patientes had COPD (FEV 1 , 69±3% ref.; DLCO, 67±5% ref.) and 18 were only smokers (FEV 1 , 92±3% ref.; DLCO, 86±4% ref.). There was no difference in the prevalence of cardiovascular risk factors between groups. The expression of TNC and EDA-FN (mean±SEM) in COPD group was 17,6±6 and 5,1±1 respectively, versus 15,5±5 and 3,9±1 in the control group (p NS). In multivariate analysis, only the active smoking was associated with higher expression of TNC (s= 24,588; p=0,002) but not with the COPD condition. CONCLUSIONS In our study, there were no differences in the gene expression of TNC and EDA-FN in lung tissue of COPD patients compared to smokers without COPD. However, we found an increased expression of TNC in relation to active smoking, so it might have a role in the pathogenesis of COPD, although the mechanisms involved in cardiovascular disease require other specific studies. Funded by FUCAP 2011.