Cigarette smoke-mediated oxidative stress induces apoptosis via the MAPKs/ XXXX pathway in @entity19 lung fibroblasts.

@entity1 @entity1380 @entity32 @entity10178 @entity14160 @entity19 @entity1995 @entity3542 @entity185 @entity6172 @entity7361 @entity777 @entity14032 @entity1379 @entity1030 @entity16279 @entity637 @entity1981 @entity8837
UNASSIGNED: Cigarette smoking is the major aetiologic factor in @entity1030 ( @entity1030 ). Lung fibroblasts are key @entity1 in the maintenance of the extracellular matrix within the lung parenchyma. However, it still remains unknown how pulmonary fibroblasts are affected by cigarette smoking. Therefore, in this study, we isolated lung fibroblasts from @entity19 and determined the apoptotic mechanism in response to @entity1981 ( @entity1981 ). When the lung fibroblasts were exposed to @entity1981 , the generation of ROS was increased as shown by @entity7361 staining and Flow Cytometry. By immunocytochemistry, @entity14160 expressing cells gradually decreased in a dose-dependent manner. The @entity3542 concentration in the supernatants increased, while the SOD activity and @entity6172 recycling decreased in response to @entity1981 . @entity1981 increased the mRNA levels of @entity637 and @entity10178 , and the secretory proteins @entity637 and @entity777 increased as measured by ELISA. We next determined whether this inflammatory process is associated with the @entity1380 / @entity1379 apoptosis pathway. The @entity1380 / @entity1379 mRNA ratio increased, and cleaved @entity185 protein was activated in the lung fibroblasts treated with @entity1981 . Moreover, @entity1981 induced the phosphorylation of @entity16279 at Tyr701/Ser727 and increased the activation of @entity8837 , @entity1995 , and @entity14032 in the MAPK pathway. Taken together, these data suggest that @entity1981 -mediated @entity32 alters the redox regulation via the MAPK- @entity16279 pathway, leading to intrinsic apoptosis of lung fibroblasts.
