tetano
Editor, Senior Moderator
J Gen Virol. 2016 Oct 20. doi: 10.1099/jgv.0.000625. [Epub ahead of print]
[h=1]The NS1 protein of avian influenza virus H9N2 induces oxidative stress-mediated chicken oviduct epithelial cells (COECs) apoptosis.[/h] Qi X[SUP]1[/SUP], Zhang H[SUP]2[/SUP], Wang Q[SUP]3[/SUP], Wang J[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The pathogenesis of H9N2 subtype avian influenza virus infection (AIV) in the hens is often related to the oviduct tissue damage. The viral nonstructural NS1 protein is thought to play key role in regulating the pathogenicity of AIV, but the exact function to this process remains elusive. In this study, the pro-apoptosis effect of H9N2 NS1 protein was examined on chicken oviduct epithelial cells (COECs) and our data suggested that NS1 induced oxidative stress was a contributing factor for apoptosis. Our data suggest that NS1 protein level was correlated with reactive oxygen species (ROS) in COECs cells transfected with NS1 expression plasmids. Interestingly, a decreased activities of antioxidant enzymes, SOD and catalase, was observed in NS1-transfected COECs. Treatment of COECs with antioxidants such as pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) significantly inhibited NS1-induced apoptosis. Moreover, although antioxidant treatment has little effect on the activation of caspase-8 in NS1-transfected cells, the activation of caspase-3/9 and Bax/Bcl-2 were significantly down-regulated. Taken together, our study demonstrated that expression of H9N2 NS1 alone is sufficient to trigger oxidative stress in COECs. Additionally, NS1 protein can induce cellular apoptosis via activating ROS accumulation and mitochondria-mediated apoptotic signaling in COECs.
PMID: 27902334 DOI: 10.1099/jgv.0.000625
[PubMed - as supplied by publisher]
[h=1]The NS1 protein of avian influenza virus H9N2 induces oxidative stress-mediated chicken oviduct epithelial cells (COECs) apoptosis.[/h] Qi X[SUP]1[/SUP], Zhang H[SUP]2[/SUP], Wang Q[SUP]3[/SUP], Wang J[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The pathogenesis of H9N2 subtype avian influenza virus infection (AIV) in the hens is often related to the oviduct tissue damage. The viral nonstructural NS1 protein is thought to play key role in regulating the pathogenicity of AIV, but the exact function to this process remains elusive. In this study, the pro-apoptosis effect of H9N2 NS1 protein was examined on chicken oviduct epithelial cells (COECs) and our data suggested that NS1 induced oxidative stress was a contributing factor for apoptosis. Our data suggest that NS1 protein level was correlated with reactive oxygen species (ROS) in COECs cells transfected with NS1 expression plasmids. Interestingly, a decreased activities of antioxidant enzymes, SOD and catalase, was observed in NS1-transfected COECs. Treatment of COECs with antioxidants such as pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) significantly inhibited NS1-induced apoptosis. Moreover, although antioxidant treatment has little effect on the activation of caspase-8 in NS1-transfected cells, the activation of caspase-3/9 and Bax/Bcl-2 were significantly down-regulated. Taken together, our study demonstrated that expression of H9N2 NS1 alone is sufficient to trigger oxidative stress in COECs. Additionally, NS1 protein can induce cellular apoptosis via activating ROS accumulation and mitochondria-mediated apoptotic signaling in COECs.
PMID: 27902334 DOI: 10.1099/jgv.0.000625
[PubMed - as supplied by publisher]