which disappearance of lung tissue

which disappearance of lung tissue in COPD may involve the progressive loss of capillary endothelial and alveolar epithelial cells through the process of apoptosis [22]. VEGF induces endothelial cell proliferation, and withdrawal of VEGF leads to endothelial cell apoptosis in vitro and in vivo [23]. Thus, VEGF is a trophic factor required for the survival of endothelial cells. Koyama et al. reported that the reduced levels of VEGF in bronchoalveolar lavage fluid were found in smokers [24]. Moreover, Kasahara et al. have reported that the protein levels and mRNA expression of both VEGF and VEGF receptor were decreased in lungs from patients with COPD, and that a decrease of VEGF action has a part of the pathogenesis of COPD [17]. However, it is unknown whether reduction in pulmonary endothelial cells leads to subsequent loss of alveolar epithelial cells. If VEGF is critical for maintenance of the alveolar compartment, and there is less alveolar compartment tissue in COPD patients, one might expect VEGF levels to be reduced, since there would be fewer distal alveolar septa that require VEGF signaling. Thus, it is still unclear whether the decrease in VEGF expression is a cause or consequence of COPD. Studies in animal models suggest that VEGF and its receptors play a protective role in the development of emphysema. For example, Kasahara et al. have shown that inhibition of VEGF receptors with the specific receptor inhibitor SU5416 can cause alveolar cell apoptosis and the development of emphysema in rats [25]. Theses findings suggest that VEGF and its receptor system may contribute to the maintenance of endothelial and epithelial cell viability.Vascular Theory in the Pathogenesis o