Newcastle disease virus-induced autophagy mediates antiapoptotic signaling responses in vitro and in vivo.
Identifieur interne : 000D05 ( Main/Exploration ); précédent : 000D04; suivant : 000D06Newcastle disease virus-induced autophagy mediates antiapoptotic signaling responses in vitro and in vivo.
Auteurs : Yinfeng Kang [République populaire de Chine] ; Runyu Yuan [République populaire de Chine] ; Bin Xiang [République populaire de Chine] ; Xiaqiong Zhao [République populaire de Chine] ; Pei Gao [République populaire de Chine] ; Xu Dai [République populaire de Chine] ; Ming Liao [République populaire de Chine] ; Tao Ren [République populaire de Chine]Source :
- Oncotarget [ 1949-2553 ] ; 2017.
Abstract
In this study, we investigated the role of autophagy and apoptosis in Newcastle disease virus (NDV)-infected chicken cells and tissues. NDV-infected and starvation-induced chick embryo fibroblasts (CEF) cells showed higher autophagosome formation than mock-infected CEF cells on transmission electron microscopy. The NDV-infected CEF cells showed enhanced conversion of microtubule-associated protein 1 light chain 3-I (LC3-I) to LC3-II and degradation of p62/SQSTM1. The diminished conversion of LC3-I to LC3-II and cleaved caspase 3 and poly (ADP-ribose) polymerase (PARP) in ultraviolet-inactivated NDV-infected cells suggested that autophagosome formation was necessary for NDV replication. Inhibition of autophagy by chloroquine (CQ) enhanced apoptosis resulting in increased cleavage of caspase 3 and PARP and AnnexinV/propidium iodide staining. Autophagy induction by rapamycin resulted in upregulation of all autophagy-related genes except Beclin 1, anti-apoptosis factors, and proinflammatory cytokines in the NDV-infected spleen and lung tissues. Subsequently, decreased apoptosis was observed in NDV-infected spleens and lungs than mock-infected organs. The pan-caspase inhibitor ZVAD-FMK promoted conversion of LC3-I to LC3-II, the degradation of p62/SQSTM1, NDV replication and cell viability by inhibiting apoptosis. Our study demonstrates that apoptosis inhibition enhances autophagy and promoted cell survival and NDV replication.
DOI: 10.18632/oncotarget.18169
PubMed: 29088762
Affiliations:
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Agricultural University, Guangzhou, 510642, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642</wicri:regionArea><wicri:noRegion>510642</wicri:noRegion></affiliation></author><author><name sortKey="Yuan, Runyu" sort="Yuan, Runyu" uniqKey="Yuan R" first="Runyu" last="Yuan">Runyu Yuan</name><affiliation wicri:level="1"><nlm:affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 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Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642</wicri:regionArea><wicri:noRegion>510642</wicri:noRegion></affiliation></author><author><name sortKey="Gao, Pei" sort="Gao, Pei" uniqKey="Gao P" first="Pei" last="Gao">Pei Gao</name><affiliation wicri:level="1"><nlm:affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642</wicri:regionArea><wicri:noRegion>510642</wicri:noRegion></affiliation></author><author><name sortKey="Dai, Xu" sort="Dai, Xu" uniqKey="Dai X" first="Xu" last="Dai">Xu Dai</name><affiliation wicri:level="1"><nlm:affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642</wicri:regionArea><wicri:noRegion>510642</wicri:noRegion></affiliation></author><author><name sortKey="Liao, Ming" sort="Liao, Ming" uniqKey="Liao M" first="Ming" last="Liao">Ming Liao</name><affiliation wicri:level="1"><nlm:affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642</wicri:regionArea><wicri:noRegion>510642</wicri:noRegion></affiliation></author><author><name sortKey="Ren, Tao" sort="Ren, Tao" uniqKey="Ren T" first="Tao" last="Ren">Tao Ren</name><affiliation wicri:level="1"><nlm:affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642</wicri:regionArea><wicri:noRegion>510642</wicri:noRegion></affiliation></author></analytic><series><title level="j">Oncotarget</title><idno type="eISSN">1949-2553</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In this study, we investigated the role of autophagy and apoptosis in Newcastle disease virus (NDV)-infected chicken cells and tissues. NDV-infected and starvation-induced chick embryo fibroblasts (CEF) cells showed higher autophagosome formation than mock-infected CEF cells on transmission electron microscopy. The NDV-infected CEF cells showed enhanced conversion of microtubule-associated protein 1 light chain 3-I (LC3-I) to LC3-II and degradation of p62/SQSTM1. The diminished conversion of LC3-I to LC3-II and cleaved caspase 3 and poly (ADP-ribose) polymerase (PARP) in ultraviolet-inactivated NDV-infected cells suggested that autophagosome formation was necessary for NDV replication. Inhibition of autophagy by chloroquine (CQ) enhanced apoptosis resulting in increased cleavage of caspase 3 and PARP and AnnexinV/propidium iodide staining. Autophagy induction by rapamycin resulted in upregulation of all autophagy-related genes except Beclin 1, anti-apoptosis factors, and proinflammatory cytokines in the NDV-infected spleen and lung tissues. Subsequently, decreased apoptosis was observed in NDV-infected spleens and lungs than mock-infected organs. The pan-caspase inhibitor ZVAD-FMK promoted conversion of LC3-I to LC3-II, the degradation of p62/SQSTM1, NDV replication and cell viability by inhibiting apoptosis. Our study demonstrates that apoptosis inhibition enhances autophagy and promoted cell survival and NDV replication.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Kang, Yinfeng" sort="Kang, Yinfeng" uniqKey="Kang Y" first="Yinfeng" last="Kang">Yinfeng Kang</name></noRegion><name sortKey="Dai, Xu" sort="Dai, Xu" uniqKey="Dai X" first="Xu" last="Dai">Xu Dai</name><name sortKey="Gao, Pei" sort="Gao, Pei" uniqKey="Gao P" first="Pei" last="Gao">Pei Gao</name><name sortKey="Liao, Ming" sort="Liao, Ming" uniqKey="Liao M" first="Ming" last="Liao">Ming Liao</name><name sortKey="Ren, Tao" sort="Ren, Tao" uniqKey="Ren T" first="Tao" last="Ren">Tao Ren</name><name sortKey="Xiang, Bin" sort="Xiang, Bin" uniqKey="Xiang B" first="Bin" last="Xiang">Bin Xiang</name><name sortKey="Yuan, Runyu" sort="Yuan, Runyu" uniqKey="Yuan R" first="Runyu" last="Yuan">Runyu Yuan</name><name sortKey="Zhao, Xiaqiong" sort="Zhao, Xiaqiong" uniqKey="Zhao X" first="Xiaqiong" last="Zhao">Xiaqiong Zhao</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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