Neutrophil defensins enhance lung epithelial wound closure and mucin gene expression in vitro.

摘要: Human airways are frequently exposed to potentially harmful agents that cause tissue injury. Upon such injury, a repair process is initiated comprises cell migration, proliferation, and differentiation. We have previously shown human neutrophil defensins (human peptides 1-3 [HNP1-3]) induce airway epithelial proliferation. Because of the role proliferation in wound repair, we investigated effect HNP1-3 on closure mucin gene expression vitro. Using NCI-H292 cultures, demonstrated dose- time-dependent increase as well increased migration. Furthermore, caused biphasic activation mitogen-activated protein kinase extracellular-regulated 1 2 (ERK1/2). Both effects ERK1/2 were blocked by specific inhibitors MEK, whereas epidermal growth factor receptor tyrosine kinase, phosphatidylinositol 3-kinase, Src did block defensin-enhanced but not activation. Finally, mRNA encoding mucins MUC5B MUC5AC, suggesting for mucous These results indicate vitro, which involves migration production. Neutrophil appears require downstream signaling pathways.