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Cigarette Smoke Extract Decreases the Expression of Vascular Endothelial Growth Factor by Cultured Cells and Triggers Apoptosis of Pulmonary Endothelial Cells*

R. M. Tuder, MD; K. Wood; L. Taraseviciene; S. C. Flores, PhD; N. F. Voekel, MD
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*From the Departments of Pathology and Medicine, Division of Respiratory Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Rubin M. Tuder, MD, Division of Pulmonary Science and Critical Care Medicine, University of Colorado Health Sciences Center, 4200 East 9th Ave, Denver, CO 80262



Chest. 2000;117(5_suppl_1):241S-242S. doi:10.1378/chest.117.5_suppl_1.241S
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Extract

Abbreviations: CSE = cigarette smoke extract; VEGF = vascular endothelial cell growth factor.

The mechanisms behind the disappearance of lung tissue (“vanishing lung”) in COPD remain enigmatic in spite of the commonly discussed hypotheses of lung inflammation and a protease-antiprotease imbalance. We postulate that there are cellular and molecular programs that maintain the structure of the adult lung. One or several of such lung cell maintenance programs, in particular for lung endothelial cells, is disrupted by the toxic effect of chronic cigarette smoke in genetically susceptible patients, thus resulting in centrilobular emphysema. Specifically, we hypothesize that disappearance of lung alveoli resulting in centrilobular emphysema occurs by apoptosis after decreased expression or activity of lung vascular endothelial cell growth factor (VEGF) or its receptors due to smoking. In the present work, we focused on the effect of cigarette smoke extract (CSE) on VEGF gene expression, on endothelial cell apoptosis, and on the ratio of the transcription factors Sp1 and Sp3, which are involved in the regulation of VEGF receptor kinase domain receptor expression in endothelial cells.

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