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Newcastle disease virus-induced autophagy mediates antiapoptotic signaling responses in vitro and in vivo.

Identifieur interne : 000787 ( Main/Exploration ); précédent : 000786; suivant : 000788

Newcastle 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 :

RBID : pubmed:29088762

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
PubMed Central: PMC5650317


Affiliations:


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<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>
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<AbstractText>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.</AbstractText>
</Abstract>
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<LastName>Kang</LastName>
<ForeName>Yinfeng</ForeName>
<Initials>Y</Initials>
<AffiliationInfo>
<Affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Department of Experimental Research, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Yuan</LastName>
<ForeName>Runyu</ForeName>
<Initials>R</Initials>
<AffiliationInfo>
<Affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory for Repository and Application of Pathogenic Microbiology, Research Center for Pathogens Detection Technology of Emerging Infectious Diseases, Guangdong Provincial Center for Disease Control and Prevention, Guangzhou, 511430, China.</Affiliation>
</AffiliationInfo>
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<LastName>Xiang</LastName>
<ForeName>Bin</ForeName>
<Initials>B</Initials>
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<Affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China.</Affiliation>
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<LastName>Zhao</LastName>
<ForeName>Xiaqiong</ForeName>
<Initials>X</Initials>
<AffiliationInfo>
<Affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China.</Affiliation>
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<ForeName>Pei</ForeName>
<Initials>P</Initials>
<AffiliationInfo>
<Affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China.</Affiliation>
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<LastName>Dai</LastName>
<ForeName>Xu</ForeName>
<Initials>X</Initials>
<AffiliationInfo>
<Affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China.</Affiliation>
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<LastName>Liao</LastName>
<ForeName>Ming</ForeName>
<Initials>M</Initials>
<AffiliationInfo>
<Affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Ren</LastName>
<ForeName>Tao</ForeName>
<Initials>T</Initials>
<AffiliationInfo>
<Affiliation>College of Veterinary Medicine, Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, Guangzhou, 510642, China.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
<PublicationTypeList>
<PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic">
<Year>2017</Year>
<Month>05</Month>
<Day>25</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo>
<Country>United States</Country>
<MedlineTA>Oncotarget</MedlineTA>
<NlmUniqueID>101532965</NlmUniqueID>
<ISSNLinking>1949-2553</ISSNLinking>
</MedlineJournalInfo>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Newcastle disease virus</Keyword>
<Keyword MajorTopicYN="N">apoptosis</Keyword>
<Keyword MajorTopicYN="N">autophagy</Keyword>
<Keyword MajorTopicYN="N">relationship</Keyword>
<Keyword MajorTopicYN="N">replication</Keyword>
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<CoiStatement>CONFLICTS OF INTEREST The authors declare that no competing interests exist.</CoiStatement>
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<Year>2017</Year>
<Month>02</Month>
<Day>09</Day>
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<Year>2017</Year>
<Month>05</Month>
<Day>12</Day>
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<Year>2017</Year>
<Month>11</Month>
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