RESUMEN
BACKGROUND: H7N9, emerged as an avian influenza virus outbreak in Eastern China in early 2013, and represented another major threat to global health. Roles of its NS1 protein, an essential viral factor, in regulating apoptosis remain unknown. METHODS: Apoptotic effect and features of H7N9/NS1 in the human A549 alveolar basal epithelial cell line were examined by caspase 3/7 activity assay and western blotting of apoptotic associated proteins. Effects of H7N9/NS1on mitochondrial membrane potential were investigated by flow cytometry. RESULTS: The expression of H7N9/NS1 in A549 cells activated caspase 3/7 and increased the protein levels of cleaved caspase 7 and cleaved poly (ADP-ribose) polymerase (PARP). H7N9/NS1-expressing A549 cells displayed a decrease in mitochondrial membrane potential. In addition, H7N9/NS1 increased the protein levels of total p53, p53 phosphorylated at Ser46 and Ser37, activated caspase 9, and the Bax/Bcl-2 ratio. CONCLUSION: Our results suggest that H7N9/NS1 protein causes the accumulation of p53 by increasing phosphorylation levels of p53 and the induction of mitochondrial dysfunction, which may contribute to H7N9/NS1-induced apoptosis in A549 cells.