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Inhibition of Vascular Endothelial Growth Factor Receptors Causes Emphysema in Rats*

Rubin M. Tuder, MD; Yasanori Kasahara, MD; Norbert F. Voelkel
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*From the University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Rubin M. Tuder, MD, University of Colorado Health Sciences Center, 4200 East 9th Ave, Denver, CO 80262



Chest. 2000;117(5_suppl_1):281S. doi:10.1378/chest.117.5_suppl_1.281S
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Abbreviations: KDR = kinase insert domain-containing receptor; VEGF = vascular endothelial growth factor

Vascular endothelial growth factor (VEGF) is perhaps the most important growth factor for endothelial cells. This growth factor is abundantly expressed in many different lung cells, including alveolar macrophages and type II cells. It acts through two different receptors that are mainly expressed on endothelial cells, kinase insert domain-containing receptor (KDR) and fetal liver tyrosine kinase. These receptor kinases affect intracellular calcium levels, and activation of KDR results in activation of the endothelial nitric oxide synthase and up-regulation of nitric oxide production. Since its discovery in cancers, the role of VEGF as an angiogenesis factor has been widely accepted. The abundance of VEGF expressed in normal lung tissue raises the question of a physiologic role for VEGF in the lung. We wondered whether VEGF not only is an endothelial cell growth factor, but perhaps also a survival factor for endothelial cells in the lung, particularly since VEGF-receptor blockade causes apoptosis in cultured endothelial cells. If indeed the signal transduction via VEGF and its receptor KDR is of principle importance for the maintenance of pulmonary endothelial cells, then chronic inhibition of VEGF receptors should lead to endothelial cell apoptosis and perhaps to emphysema.

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