TY - JOUR T1 - The transcription factor slug is increased in pulmonary artery endothelial cells of COPD patients JF - European Respiratory Journal JO - Eur Respir J VL - 42 IS - Suppl 57 SP - P5163 AU - Nuria Coll AU - Victor Peinado AU - Jessica Garcia AU - Borja Lobo AU - David Dominguez AU - Joan Albert Barbera AU - Melina Mara Musri Y1 - 2013/09/01 UR - http://erj.ersjournals.com/content/42/Suppl_57/P5163.abstract N2 - Slug is a transcription factor driving the trans-differentiation of endothelial cells (EC) into mesenchymal cells in a mechanism called endothelial to mesenchymal transition (EnMT).This process, which may play a role in the intimal thickening of pulmonary arteries in COPD, can be potentiated by an inflammatory environment. The aim of this study was twofold, first to evaluate the expression of slug in EC of pulmonary arteries from COPD patients and second to asses in vitro the gene expression profile related with EnMT in cultured EC exposed to inflammatory cytokines. The expression of slug was studied by immunohistochemistry in arterial sections of isolated pulmonary arteries from COPD patients (n=4) and controls subjects (n=5). The number of positive endothelial cells was related to the luminal perimeter. In the other set of experiments, human pulmonary artery endothelial cells were incubated in presence of TNFα (10ng/ml) for 24h and the gene expression of EnMT markers were measured by real time PCR. The number of EC showing positive immunostaining to slug was higher in COPD arteries than in controls healthy subjects (1.63±1.35 cells/µm vs 0.41±0.72 cells/µm; p<0.05), respectively. TNFα increased significantly (p<0.05) two and three fold the expression of slug and snail, whereas VE-cadherin decreased. The expression of the transcription factor slug is increased in endothelial cells of pulmonary arteries from COPD patients, suggesting that these cells might contribute to vascular remodeling by an EnMT process, which might be initiated or amplified by inflammatory cytokines.Supported by grants 10/02175, and SEPAR-2009, MMM is recipient of Sara Borrell contract from ISCiii. ER -