Modulation of Caveolin-mediated NO release under inflammatory conditions in human alveolar epithelial cells

초록

Alveolar type-II epithelial cells serve as the major site of interaction between the extracellular environment and the lung. Although the cells are non-immune cell type, they respond to acute and chronic stimuli by releasing inflammatory mediators like cytokines, nitric oxide(NO) and prostaglandin E2(PGE2). This study was designed to study the role of NO overproduced by the human alveolar type-II epithelial cells stimulated by mixture of bacterial lipopolysaccharide(LPS) and inflammatory cytokines mimicking extracellular enveironmental stimuli. In particular, the role of NO in modulating the expression of CaV-1, a typical inhibitory protein on NO production catalyzed by nNOS and Enos, in alveolar epithelial cells was examined. Under inflammatory conditions, expressions of the NO Producing NOSs and elevated or aaattenuated along with increase of CaV-1 expression in human alveolar epithelial cells(normal embroyonic L132 and adenocarcinoma A549 cells) While the overall ability to produce NO was increased markedlyby Ca++- independent iNOS there was a significant decrease in Ca++-dependent Nnos and eNOSactivities and the latter was associated with enhanced CaV-1 expression.