Influenza A virus PB1-F2 is involved in regulation of cellular redox state in alveolar epithelial cells.
Identifieur interne : 000433 ( PubMed/Curation ); précédent : 000432; suivant : 000434Influenza A virus PB1-F2 is involved in regulation of cellular redox state in alveolar epithelial cells.
Auteurs : Nary Shin [Corée du Sud] ; Chul-Woong Pyo [Corée du Sud] ; Kwang Il Jung [Corée du Sud] ; Sang-Yun Choi [Corée du Sud]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2015.
Descripteurs français
- KwdFr :
- Alvéoles pulmonaires (cytologie), Alvéoles pulmonaires (enzymologie), Alvéoles pulmonaires (métabolisme), Animaux, Cellules rénales canines Madin-Darby, Chiens, Espèces réactives de l'oxygène (métabolisme), Humains, Lignée cellulaire, Oxydoréduction, Protéines virales (physiologie), RT-PCR, Superoxide dismutase (métabolisme), Superoxide dismutase-1.
- MESH :
- cytologie : Alvéoles pulmonaires.
- enzymologie : Alvéoles pulmonaires.
- métabolisme : Alvéoles pulmonaires, Espèces réactives de l'oxygène, Superoxide dismutase.
- physiologie : Protéines virales.
- Animaux, Cellules rénales canines Madin-Darby, Chiens, Humains, Lignée cellulaire, Oxydoréduction, RT-PCR, Superoxide dismutase-1.
English descriptors
- KwdEn :
- Animals, Cell Line, Dogs, Humans, Madin Darby Canine Kidney Cells, Oxidation-Reduction, Pulmonary Alveoli (cytology), Pulmonary Alveoli (enzymology), Pulmonary Alveoli (metabolism), Reactive Oxygen Species (metabolism), Reverse Transcriptase Polymerase Chain Reaction, Superoxide Dismutase (metabolism), Superoxide Dismutase-1, Viral Proteins (physiology).
- MESH :
- chemical , metabolism : Reactive Oxygen Species, Superoxide Dismutase.
- cytology : Pulmonary Alveoli.
- enzymology : Pulmonary Alveoli.
- metabolism : Pulmonary Alveoli.
- chemical , physiology : Viral Proteins.
- Animals, Cell Line, Dogs, Humans, Madin Darby Canine Kidney Cells, Oxidation-Reduction, Reverse Transcriptase Polymerase Chain Reaction, Superoxide Dismutase-1.
Abstract
Occurrence of oxidative stress is common in influenza, and renders the host more susceptible to pathogenic effects including cell death. We previously reported that down-regulation of superoxide anion dismutase 1 (SOD1) by influenza A virus (IAV) resulted in a significant increase in the levels of reactive oxygen species (ROS) and viral PB1 polymerase gene product in the early stage of infection. However, the precise molecular mechanism of IAV-mediated ROS generation is not yet fully understood. In this study, we investigated the possible involvement of the key virulence factor PB1-F2 in ROS generation and its contribution to the viral propagation and cell death. The key virulence factor PB1-F2 was found to be responsible, at least in part, for the ROS generation through lowering the SOD1 level in alveolar epithelial A549 cells. PB1-F2 overexpression resulted in SOD1 diminishment and ROS enhancement, while another virulent factor, NS1, did not show significant changes. Inversely, we examined the effects of the absence of PB1-F2 using mutant IAV lacking PB1-F2 expression (mutantΔF2). Infection with mutantΔF2 virus did not significantly lower the SOD1 level, and thus generated moderately low levels of ROS. In addition, the oxidative activity of PB1-F2 was directly reflected by cell viability and death. Infection with the mutant virus reduced the percentage of apoptotic cells more than two-fold compared to the wild-type IAV in A549 cells. Furthermore, expression of exogenous SOD1 gene abrogated a large portion of the PB1-F2-induced apoptosis of cells infected with wild-type IAV, but affected much less of the mutantΔF2 virus-infected cells. These results suggest that the PB1-F2 is directly implicated in virus-induced oxidative stress, thereby contributing to the early stages of IAV replication cycle and ultimately to disease severity.
DOI: 10.1016/j.bbrc.2015.03.010
PubMed: 25769947
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We previously reported that down-regulation of superoxide anion dismutase 1 (SOD1) by influenza A virus (IAV) resulted in a significant increase in the levels of reactive oxygen species (ROS) and viral PB1 polymerase gene product in the early stage of infection. However, the precise molecular mechanism of IAV-mediated ROS generation is not yet fully understood. In this study, we investigated the possible involvement of the key virulence factor PB1-F2 in ROS generation and its contribution to the viral propagation and cell death. The key virulence factor PB1-F2 was found to be responsible, at least in part, for the ROS generation through lowering the SOD1 level in alveolar epithelial A549 cells. PB1-F2 overexpression resulted in SOD1 diminishment and ROS enhancement, while another virulent factor, NS1, did not show significant changes. Inversely, we examined the effects of the absence of PB1-F2 using mutant IAV lacking PB1-F2 expression (mutantΔF2). Infection with mutantΔF2 virus did not significantly lower the SOD1 level, and thus generated moderately low levels of ROS. In addition, the oxidative activity of PB1-F2 was directly reflected by cell viability and death. Infection with the mutant virus reduced the percentage of apoptotic cells more than two-fold compared to the wild-type IAV in A549 cells. Furthermore, expression of exogenous SOD1 gene abrogated a large portion of the PB1-F2-induced apoptosis of cells infected with wild-type IAV, but affected much less of the mutantΔF2 virus-infected cells. These results suggest that the PB1-F2 is directly implicated in virus-induced oxidative stress, thereby contributing to the early stages of IAV replication cycle and ultimately to disease severity. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25769947</PMID><DateCompleted><Year>2015</Year><Month>06</Month><Day>05</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>459</Volume><Issue>4</Issue><PubDate><Year>2015</Year><Month>Apr</Month><Day>17</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem. Biophys. Res. Commun.</ISOAbbreviation></Journal><ArticleTitle>Influenza A virus PB1-F2 is involved in regulation of cellular redox state in alveolar epithelial cells.</ArticleTitle><Pagination><MedlinePgn>699-705</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2015.03.010</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(15)00435-0</ELocationID><Abstract><AbstractText>Occurrence of oxidative stress is common in influenza, and renders the host more susceptible to pathogenic effects including cell death. We previously reported that down-regulation of superoxide anion dismutase 1 (SOD1) by influenza A virus (IAV) resulted in a significant increase in the levels of reactive oxygen species (ROS) and viral PB1 polymerase gene product in the early stage of infection. However, the precise molecular mechanism of IAV-mediated ROS generation is not yet fully understood. In this study, we investigated the possible involvement of the key virulence factor PB1-F2 in ROS generation and its contribution to the viral propagation and cell death. The key virulence factor PB1-F2 was found to be responsible, at least in part, for the ROS generation through lowering the SOD1 level in alveolar epithelial A549 cells. PB1-F2 overexpression resulted in SOD1 diminishment and ROS enhancement, while another virulent factor, NS1, did not show significant changes. Inversely, we examined the effects of the absence of PB1-F2 using mutant IAV lacking PB1-F2 expression (mutantΔF2). Infection with mutantΔF2 virus did not significantly lower the SOD1 level, and thus generated moderately low levels of ROS. In addition, the oxidative activity of PB1-F2 was directly reflected by cell viability and death. Infection with the mutant virus reduced the percentage of apoptotic cells more than two-fold compared to the wild-type IAV in A549 cells. Furthermore, expression of exogenous SOD1 gene abrogated a large portion of the PB1-F2-induced apoptosis of cells infected with wild-type IAV, but affected much less of the mutantΔF2 virus-infected cells. These results suggest that the PB1-F2 is directly implicated in virus-induced oxidative stress, thereby contributing to the early stages of IAV replication cycle and ultimately to disease severity. </AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shin</LastName><ForeName>Nary</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Life Sciences, Korea University, Seoul 136-701, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pyo</LastName><ForeName>Chul-Woong</ForeName><Initials>CW</Initials><AffiliationInfo><Affiliation>Department of Life Sciences, Korea University, Seoul 136-701, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jung</LastName><ForeName>Kwang Il</ForeName><Initials>KI</Initials><AffiliationInfo><Affiliation>Department of Life Sciences, Korea University, Seoul 136-701, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Sang-Yun</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Department of Life Sciences, Korea University, Seoul 136-701, Republic of Korea. Electronic address: sychoi@korea.ac.kr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>03</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C442816">PB1-F2 protein, Influenza A virus</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000606290">SOD1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014764">Viral Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D000072105">Superoxide Dismutase-1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D061985" MajorTopicYN="N">Madin Darby Canine Kidney Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011650" MajorTopicYN="N">Pulmonary Alveoli</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000072105" MajorTopicYN="N">Superoxide Dismutase-1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014764" MajorTopicYN="N">Viral Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Influenza A virus</Keyword><Keyword MajorTopicYN="N">PB1-F2</Keyword><Keyword MajorTopicYN="N">ROS</Keyword><Keyword MajorTopicYN="N">Superoxide anion dismutase 1</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>01</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>03</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>3</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>3</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>6</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25769947</ArticleId><ArticleId IdType="pii">S0006-291X(15)00435-0</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2015.03.010</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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