Possible role of Kr  ppel-like factor 5 in the remodeling of small airways and pulmonary vessels in XXXX .

@entity1 @entity219 @entity120 @entity26004 @entity1030 @entity65
BACKGROUND: Small airway remodeling is an important cause of the airflow limitation in @entity1030 ( @entity1030 ). A large population of @entity1 with @entity1030 also have @entity120 . Kr  ppel-like factor 5 ( @entity26004 ) is a @entity219 -finger transcription factor that contributes to tissue remodeling in @entity65 . Here, we evaluate the possible involvement of @entity26004 in the remodeling of small airways and pulmonary vessels in @entity1030 . METHODS: Lung tissues were obtained from 23 control never-smokers, 17 control ex-smokers and 24 ex-smokers with @entity1030 . The expression of @entity26004 in the lung tissues was investigated by immunohistochemistry. We investigated whether oxidative/nitrosative stress, which is a major cause of the pathogenesis in @entity1030 , could augment the production of @entity26004 . We examined the role of @entity26004 in the stress-mediated tissue remodeling responses. We also investigated the susceptibility of @entity26004 expression to nitrosative stress using bronchial fibroblasts isolated from the lung tissues. RESULTS: The expression of @entity26004 was up-regulated in the small airways and pulmonary vessels of the @entity1030 @entity1 and it was mainly expressed in bronchial fibroblasts and cells of the pulmonary vessels. The extent of the @entity26004 expression in the small airway of the @entity1030 group had a significant correlation with the severity of the airflow limitation. Oxidative/nitrosative stress augmented the production of @entity26004 in lung fibroblasts as well as the translocation of @entity26004 into the nuclei. Silencing of @entity26004 suppressed the stress-augmented differentiation into myofibroblasts, the release of collagens and metalloproteinases. Bronchial fibroblasts from the @entity1 with @entity1030 highly expressed @entity26004 compared to those from the control subjects under basal condition and were more susceptible to the induction of @entity26004 expression by nitrosative stress compared to those from the control subjects. CONCLUSION: We provide the first evidence that the expression of @entity26004 is up-regulated in small airways and pulmonary vessels of @entity1 with @entity1030 and may be involved in the tissue remodeling of @entity1030 .
