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Am. J. Respir. Crit. Care Med., Volume 163, Number 3, March 2001, 737-744

Endothelial Cell Death and Decreased Expression of Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor 2 in Emphysema

YASUNORI KASAHARA, RUBIN M. TUDER, CARLYNE D. COOL, DAVID A. LYNCH, SONIA C. FLORES, and NORBERT F. VOELKEL

Division of Pulmonary Sciences and Critical Care Medicine, Pulmonary Hypertension Center, Department of Pathology, Department of Radiology, and Webb-Waring Antioxidant Research Institute, University of Colorado Health Sciences Center, Denver, Colorado

Emphysema due to cigarette smoking is characterized by a loss of alveolar structures. We hypothesize that the disappearance of alveoli involves apoptosis of septal endothelial cells and a decreased expression of lung vascular endothelial growth factor (VEGF) and its receptor 2 (VEGF R2). By terminal transferase dUTP nick end labeling (TUNEL) in combination with immunohistochemistry, we found that the number of TUNEL+ septal epithelial and endothelial cells/lung tissue nucleic acid (µg) was increased in the alveolar septa of emphysema lungs (14.2 ± 2.0/µg, n = 6) when compared with normal lungs (6.8 ± 1.3/µg, n = 7) (p < 0.01) and with primary pulmonary hypertensive lungs (2.3 ± 0.8/µg, n = 5) (p < 0.001). The cell death events were not significantly different between healthy nonsmoker (7.4 ± 1.9/µg) and smoker (5.7 ± 0.7/µg) control subjects. The TUNEL results were confirmed by single-stranded DNA and active caspase-3 immunohistochemistry, and by DNA ligation assay. Emphysema lungs (n = 12) had increased levels of oligonucleosomal-length DNA fragmentation when compared with normal lungs (n = 11). VEGF, VEGF R2 protein, and mRNA expression were significantly reduced in emphysema. We propose that epithelial and endothelial alveolar septal death due to a decrease of endothelial cell maintenance factors may be part of the pathogenesis of emphysema.




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