Mechanisms of establishment of persistent SARS-CoV-infected cells.
Identifieur interne : 001555 ( Ncbi/Merge ); précédent : 001554; suivant : 001556Mechanisms of establishment of persistent SARS-CoV-infected cells.
Auteurs : Tetsuya Mizutani [Japon] ; Shuetsu Fukushi ; Koji Ishii ; Yuko Sasaki ; Tsuyoshi Kenri ; Masayuki Saijo ; Yumi Kanaji ; Kinji Shirota ; Ichiro Kurane ; Shigeru MorikawaSource :
- Biochemical and biophysical research communications [ 0006-291X ] ; 2006.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Cytokines, Syndrome respiratoire aigu sévère.
- physiologie : Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Apoptose, Cellules Vero, Survie cellulaire, Techniques de culture cellulaire.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Cytokines.
- metabolism : Severe Acute Respiratory Syndrome.
- methods : Cell Culture Techniques.
- physiology : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Apoptosis, Cell Survival, Chlorocebus aethiops, Vero Cells.
Abstract
Previously, we reported the establishment of cells with persistent SARS-CoV infection after apoptotic events and showed that both JNK and PI3K/Akt signaling pathways are important for persistence by treatment with inhibitors at the early stages of SARS-CoV infection. However, the mechanisms of establishment of persistent infection are still unclear. In this study, we investigated which signaling pathways play important roles in escape from apoptosis in cells infected with SARS-CoV. In persistently infected cells at 50h.p.i., PI3K/Akt, JNK, p38 MAPK and Bcl-2 were phosphorylated and the protein levels of Bcl-2 and Bcl-xL were increased. When surviving cells were treated with the JNK-specific inhibitor, SP600125, at 50h.p.i., all cells died, suggesting that the JNK signaling pathway is necessary for maintenance of persistently infected cells. Among the signaling pathways in persistently infected cells, Akt and JNK were phosphorylated in SARS-CoV-nucleocapsid (N) protein-expressing Vero E6 cells using vaccinia viral vector (DIs), strongly suggesting that N protein-induced phosphorylation of Akt and JNK are necessary to establish persistence. These results indicated that at least four proteins, Akt, JNK, Bcl-2 and Bcl-xL, are necessary for survival of persistently SARS-CoV-infected cells.
DOI: 10.1016/j.bbrc.2006.06.086
PubMed: 16808902
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last="Mizutani">Tetsuya Mizutani</name><affiliation wicri:level="3"><nlm:affiliation>Department of Virology 1, National Institute of Infectious Diseases, Musashimurayama, Tokyo, Japan. tmizutan@nih.go.jp</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Virology 1, National Institute of Infectious Diseases, Musashimurayama, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Fukushi, Shuetsu" sort="Fukushi, Shuetsu" uniqKey="Fukushi S" first="Shuetsu" last="Fukushi">Shuetsu Fukushi</name></author><author><name sortKey="Ishii, Koji" sort="Ishii, Koji" uniqKey="Ishii K" first="Koji" last="Ishii">Koji Ishii</name></author><author><name sortKey="Sasaki, Yuko" sort="Sasaki, Yuko" uniqKey="Sasaki Y" first="Yuko" last="Sasaki">Yuko Sasaki</name></author><author><name sortKey="Kenri, Tsuyoshi" sort="Kenri, Tsuyoshi" uniqKey="Kenri T" first="Tsuyoshi" last="Kenri">Tsuyoshi Kenri</name></author><author><name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</name></author><author><name sortKey="Kanaji, Yumi" sort="Kanaji, Yumi" uniqKey="Kanaji Y" first="Yumi" last="Kanaji">Yumi Kanaji</name></author><author><name sortKey="Shirota, Kinji" sort="Shirota, Kinji" uniqKey="Shirota K" first="Kinji" last="Shirota">Kinji Shirota</name></author><author><name sortKey="Kurane, Ichiro" sort="Kurane, Ichiro" uniqKey="Kurane I" first="Ichiro" last="Kurane">Ichiro Kurane</name></author><author><name sortKey="Morikawa, Shigeru" sort="Morikawa, Shigeru" uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="ISSN">0006-291X</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Cell Culture Techniques (methods)</term><term>Cell Survival</term><term>Chlorocebus aethiops</term><term>Cytokines (metabolism)</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (metabolism)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Vero Cells</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Cellules Vero</term><term>Cytokines (métabolisme)</term><term>Survie cellulaire</term><term>Syndrome respiratoire aigu sévère (métabolisme)</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Techniques de culture cellulaire ()</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Cell Culture Techniques</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Cell Survival</term><term>Chlorocebus aethiops</term><term>Vero Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Cellules Vero</term><term>Survie cellulaire</term><term>Techniques de culture cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previously, we reported the establishment of cells with persistent SARS-CoV infection after apoptotic events and showed that both JNK and PI3K/Akt signaling pathways are important for persistence by treatment with inhibitors at the early stages of SARS-CoV infection. However, the mechanisms of establishment of persistent infection are still unclear. In this study, we investigated which signaling pathways play important roles in escape from apoptosis in cells infected with SARS-CoV. In persistently infected cells at 50h.p.i., PI3K/Akt, JNK, p38 MAPK and Bcl-2 were phosphorylated and the protein levels of Bcl-2 and Bcl-xL were increased. When surviving cells were treated with the JNK-specific inhibitor, SP600125, at 50h.p.i., all cells died, suggesting that the JNK signaling pathway is necessary for maintenance of persistently infected cells. Among the signaling pathways in persistently infected cells, Akt and JNK were phosphorylated in SARS-CoV-nucleocapsid (N) protein-expressing Vero E6 cells using vaccinia viral vector (DIs), strongly suggesting that N protein-induced phosphorylation of Akt and JNK are necessary to establish persistence. These results indicated that at least four proteins, Akt, JNK, Bcl-2 and Bcl-xL, are necessary for survival of persistently SARS-CoV-infected cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16808902</PMID><DateCompleted><Year>2006</Year><Month>09</Month><Day>13</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0006-291X</ISSN><JournalIssue CitedMedium="Print"><Volume>347</Volume><Issue>1</Issue><PubDate><Year>2006</Year><Month>Aug</Month><Day>18</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem. Biophys. Res. Commun.</ISOAbbreviation></Journal><ArticleTitle>Mechanisms of establishment of persistent SARS-CoV-infected cells.</ArticleTitle><Pagination><MedlinePgn>261-5</MedlinePgn></Pagination><Abstract><AbstractText>Previously, we reported the establishment of cells with persistent SARS-CoV infection after apoptotic events and showed that both JNK and PI3K/Akt signaling pathways are important for persistence by treatment with inhibitors at the early stages of SARS-CoV infection. However, the mechanisms of establishment of persistent infection are still unclear. In this study, we investigated which signaling pathways play important roles in escape from apoptosis in cells infected with SARS-CoV. In persistently infected cells at 50h.p.i., PI3K/Akt, JNK, p38 MAPK and Bcl-2 were phosphorylated and the protein levels of Bcl-2 and Bcl-xL were increased. When surviving cells were treated with the JNK-specific inhibitor, SP600125, at 50h.p.i., all cells died, suggesting that the JNK signaling pathway is necessary for maintenance of persistently infected cells. Among the signaling pathways in persistently infected cells, Akt and JNK were phosphorylated in SARS-CoV-nucleocapsid (N) protein-expressing Vero E6 cells using vaccinia viral vector (DIs), strongly suggesting that N protein-induced phosphorylation of Akt and JNK are necessary to establish persistence. These results indicated that at least four proteins, Akt, JNK, Bcl-2 and Bcl-xL, are necessary for survival of persistently SARS-CoV-infected cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mizutani</LastName><ForeName>Tetsuya</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Virology 1, National Institute of Infectious Diseases, Musashimurayama, Tokyo, Japan. tmizutan@nih.go.jp</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fukushi</LastName><ForeName>Shuetsu</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Ishii</LastName><ForeName>Koji</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Sasaki</LastName><ForeName>Yuko</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Kenri</LastName><ForeName>Tsuyoshi</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Saijo</LastName><ForeName>Masayuki</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Kanaji</LastName><ForeName>Yumi</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Shirota</LastName><ForeName>Kinji</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Kurane</LastName><ForeName>Ichiro</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Morikawa</LastName><ForeName>Shigeru</ForeName><Initials>S</Initials></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>2006</Year><Month>06</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res 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first="Yumi" last="Kanaji">Yumi Kanaji</name><name sortKey="Kenri, Tsuyoshi" sort="Kenri, Tsuyoshi" uniqKey="Kenri T" first="Tsuyoshi" last="Kenri">Tsuyoshi Kenri</name><name sortKey="Kurane, Ichiro" sort="Kurane, Ichiro" uniqKey="Kurane I" first="Ichiro" last="Kurane">Ichiro Kurane</name><name sortKey="Morikawa, Shigeru" sort="Morikawa, Shigeru" uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name><name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</name><name sortKey="Sasaki, Yuko" sort="Sasaki, Yuko" uniqKey="Sasaki Y" first="Yuko" last="Sasaki">Yuko Sasaki</name><name sortKey="Shirota, Kinji" sort="Shirota, Kinji" uniqKey="Shirota K" first="Kinji" last="Shirota">Kinji Shirota</name></noCountry><country name="Japon"><region name="Région de Kantō"><name sortKey="Mizutani, Tetsuya" sort="Mizutani, Tetsuya" uniqKey="Mizutani T" first="Tetsuya" last="Mizutani">Tetsuya 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