The NS1 protein of avian influenza virus H9N2 induces oxidative-stress-mediated chicken oviduct epithelial cells apoptosis.
Identifieur interne : 000832 ( Ncbi/Checkpoint ); précédent : 000831; suivant : 000833The NS1 protein of avian influenza virus H9N2 induces oxidative-stress-mediated chicken oviduct epithelial cells apoptosis.
Auteurs : Xuefeng Qi [République populaire de Chine] ; Huizhu Zhang [République populaire de Chine] ; Qiuzhen Wang [République populaire de Chine] ; Jingyu Wang [République populaire de Chine]Source :
- The Journal of general virology [ 1465-2099 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Apoptose, Caspases (métabolisme), Cellules épithéliales (cytologie), Cellules épithéliales (métabolisme), Cellules épithéliales (virologie), Espèces réactives de l'oxygène (métabolisme), Femelle, Grippe chez les oiseaux (métabolisme), Grippe chez les oiseaux (physiopathologie), Grippe chez les oiseaux (virologie), Maladies de la volaille (métabolisme), Maladies de la volaille (physiopathologie), Maladies de la volaille (virologie), Mitochondries (métabolisme), Oviductes (cytologie), Oviductes (métabolisme), Oviductes (virologie), Poulets, Protéines virales non structurales (génétique), Protéines virales non structurales (métabolisme), Sous-type H9N2 du virus de la grippe A (génétique), Sous-type H9N2 du virus de la grippe A (métabolisme), Stress oxydatif.
- MESH :
- cytologie : Cellules épithéliales, Oviductes.
- génétique : Protéines virales non structurales, Sous-type H9N2 du virus de la grippe A.
- métabolisme : Caspases, Cellules épithéliales, Espèces réactives de l'oxygène, Grippe chez les oiseaux, Maladies de la volaille, Mitochondries, Oviductes, Protéines virales non structurales, Sous-type H9N2 du virus de la grippe A.
- physiopathologie : Grippe chez les oiseaux, Maladies de la volaille.
- virologie : Cellules épithéliales, Grippe chez les oiseaux, Maladies de la volaille, Oviductes.
- Animaux, Apoptose, Femelle, Poulets, Stress oxydatif.
English descriptors
- KwdEn :
- Animals, Apoptosis, Caspases (metabolism), Chickens, Epithelial Cells (cytology), Epithelial Cells (metabolism), Epithelial Cells (virology), Female, Influenza A Virus, H9N2 Subtype (genetics), Influenza A Virus, H9N2 Subtype (metabolism), Influenza in Birds (metabolism), Influenza in Birds (physiopathology), Influenza in Birds (virology), Mitochondria (metabolism), Oviducts (cytology), Oviducts (metabolism), Oviducts (virology), Oxidative Stress, Poultry Diseases (metabolism), Poultry Diseases (physiopathology), Poultry Diseases (virology), Reactive Oxygen Species (metabolism), Viral Nonstructural Proteins (genetics), Viral Nonstructural Proteins (metabolism).
- MESH :
- chemical , genetics : Viral Nonstructural Proteins.
- chemical , metabolism : Caspases, Reactive Oxygen Species, Viral Nonstructural Proteins.
- cytology : Epithelial Cells, Oviducts.
- genetics : Influenza A Virus, H9N2 Subtype.
- metabolism : Epithelial Cells, Influenza A Virus, H9N2 Subtype, Influenza in Birds, Mitochondria, Oviducts, Poultry Diseases.
- physiopathology : Influenza in Birds, Poultry Diseases.
- virology : Epithelial Cells, Influenza in Birds, Oviducts, Poultry Diseases.
- Animals, Apoptosis, Chickens, Female, Oxidative Stress.
Abstract
The pathogenesis of H9N2 subtype avian influenza virus infection (AIV) in hens is often related to oviduct tissue damage. The viral non-structural NS1 protein is thought to play a key role in regulating the pathogenicity of AIV, but its exact function in 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 indicated that NS1-induced oxidative stress was a contributing factor in apoptosis. Our data indicate that NS1 protein level was correlated with reactive oxygen species (ROS) in COECs transfected with NS1 expression plasmids. Interestingly, decreased activities of antioxidant enzymes, superoxide dismutase and catalase, were 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 downregulated. Taken together, the results of 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 signalling in COECs.
DOI: 10.1099/jgv.0.000625
PubMed: 27902334
Affiliations:
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China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Veterinary Medicine College, Northwest A&F University, Yangling 712100</wicri:regionArea><wicri:noRegion>Yangling 712100</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Qiuzhen" sort="Wang, Qiuzhen" uniqKey="Wang Q" first="Qiuzhen" last="Wang">Qiuzhen Wang</name><affiliation wicri:level="1"><nlm:affiliation>Veterinary Medicine College, Northwest A&F University, Yangling 712100, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Veterinary Medicine College, Northwest A&F University, Yangling 712100</wicri:regionArea><wicri:noRegion>Yangling 712100</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Jingyu" sort="Wang, Jingyu" uniqKey="Wang J" first="Jingyu" last="Wang">Jingyu Wang</name><affiliation wicri:level="1"><nlm:affiliation>Veterinary Medicine College, Northwest A&F University, Yangling 712100, PR China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Veterinary Medicine College, Northwest A&F University, Yangling 712100</wicri:regionArea><wicri:noRegion>Yangling 712100</wicri:noRegion></affiliation></author></analytic><series><title level="j">The Journal of general virology</title><idno type="eISSN">1465-2099</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Caspases (metabolism)</term><term>Chickens</term><term>Epithelial Cells (cytology)</term><term>Epithelial Cells (metabolism)</term><term>Epithelial Cells (virology)</term><term>Female</term><term>Influenza A Virus, H9N2 Subtype (genetics)</term><term>Influenza A Virus, H9N2 Subtype (metabolism)</term><term>Influenza in Birds (metabolism)</term><term>Influenza in Birds (physiopathology)</term><term>Influenza in Birds (virology)</term><term>Mitochondria (metabolism)</term><term>Oviducts (cytology)</term><term>Oviducts (metabolism)</term><term>Oviducts (virology)</term><term>Oxidative Stress</term><term>Poultry Diseases (metabolism)</term><term>Poultry Diseases (physiopathology)</term><term>Poultry Diseases (virology)</term><term>Reactive Oxygen Species (metabolism)</term><term>Viral Nonstructural Proteins (genetics)</term><term>Viral Nonstructural Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Caspases (métabolisme)</term><term>Cellules épithéliales (cytologie)</term><term>Cellules épithéliales (métabolisme)</term><term>Cellules épithéliales (virologie)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Femelle</term><term>Grippe chez les oiseaux (métabolisme)</term><term>Grippe chez les oiseaux (physiopathologie)</term><term>Grippe chez les oiseaux 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xml:lang="fr"><term>Cellules épithéliales</term><term>Oviductes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Epithelial Cells</term><term>Oviducts</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A Virus, H9N2 Subtype</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines virales non structurales</term><term>Sous-type H9N2 du virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term><term>Influenza A Virus, H9N2 Subtype</term><term>Influenza in Birds</term><term>Mitochondria</term><term>Oviducts</term><term>Poultry Diseases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspases</term><term>Cellules épithéliales</term><term>Espèces réactives de l'oxygène</term><term>Grippe chez les oiseaux</term><term>Maladies de la 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Stress</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Femelle</term><term>Poulets</term><term>Stress oxydatif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathogenesis of H9N2 subtype avian influenza virus infection (AIV) in hens is often related to oviduct tissue damage. The viral non-structural NS1 protein is thought to play a key role in regulating the pathogenicity of AIV, but its exact function in 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 indicated that NS1-induced oxidative stress was a contributing factor in apoptosis. Our data indicate that NS1 protein level was correlated with reactive oxygen species (ROS) in COECs transfected with NS1 expression plasmids. Interestingly, decreased activities of antioxidant enzymes, superoxide dismutase and catalase, were 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 downregulated. Taken together, the results of 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 signalling in COECs.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Qi, Xuefeng" sort="Qi, Xuefeng" uniqKey="Qi X" first="Xuefeng" last="Qi">Xuefeng Qi</name></noRegion><name sortKey="Wang, Jingyu" sort="Wang, Jingyu" uniqKey="Wang J" first="Jingyu" last="Wang">Jingyu Wang</name><name sortKey="Wang, Qiuzhen" sort="Wang, Qiuzhen" uniqKey="Wang Q" first="Qiuzhen" last="Wang">Qiuzhen Wang</name><name sortKey="Zhang, Huizhu" sort="Zhang, Huizhu" uniqKey="Zhang H" first="Huizhu" last="Zhang">Huizhu Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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