作者: Julie A. Wickenden , Murray C. H. Clarke , Adriano G. Rossi , Irfan Rahman , Stephen P. Faux
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摘要: Emphysema is characterized by enlargement of the distal airspaces in lungs due to destruction alveolar walls. Alveolar endothelial and epithelial cell apoptosis induced cigarette smoke thought be a possible mechanism for this loss. In contrast, our studies show that condensate (CSC) induces necrosis cells human umbilical vein cells. Furthermore, study death pathway model system using Jurkat revealed addition inducing necrosis, CSC inhibited staurosporine or Fas ligation, with both effects prevented antioxidants glutathione dithiothreitol. Time course experiments an early step caspase cascade, whereby caspase-3 was not activated. Moreover, cell-free reconstitution apoptosome cytoplasmic extracts from CSC-treated cells, cytochrome-c dATP, did result activation caspases-3 -9. Thus, treat...