Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells.
Identifieur interne : 002339 ( PubMed/Corpus ); précédent : 002338; suivant : 002340Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells.
Auteurs : Tetsuya Mizutani ; Shuetsu Fukushi ; Daisuke Iizuka ; Osamu Inanami ; Mikinori Kuwabara ; Hideaki Takashima ; Hiroshi Yanagawa ; Masayuki Saijo ; Ichiro Kurane ; Shigeru MorikawaSource :
- FEMS immunology and medical microbiology [ 0928-8244 ] ; 2006.
English descriptors
- KwdEn :
- Animals, Apoptosis, Cell Proliferation, Chlorocebus aethiops, Gene Expression Regulation, Glycogen Synthase Kinase 3 (genetics), Glycogen Synthase Kinase 3 (metabolism), Humans, Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), Phosphorylation, Proto-Oncogene Proteins c-akt (genetics), Proto-Oncogene Proteins c-akt (metabolism), SARS Virus (pathogenicity), Signal Transduction, Vero Cells.
- MESH :
- chemical , genetics : Glycogen Synthase Kinase 3, Proto-Oncogene Proteins c-akt.
- chemical , metabolism : Glycogen Synthase Kinase 3, Proto-Oncogene Proteins c-akt.
- genetics : Phosphatidylinositol 3-Kinases.
- metabolism : Phosphatidylinositol 3-Kinases.
- pathogenicity : SARS Virus.
- Animals, Apoptosis, Cell Proliferation, Chlorocebus aethiops, Gene Expression Regulation, Humans, Phosphorylation, Signal Transduction, Vero Cells.
Abstract
Severe acute respiratory syndrome (SARS) is caused by SARS-coronavirus (SARS-CoV). Infection of Vero E6 cells with SARS-CoV inhibits cell proliferation. Our previous study indicated that Akt, which is poorly phosphorylated in confluent cultures of Vero E6 cells, is phosphorylated and then dephosphorylated upon infection by SARS-CoV. In the present study, we showed that a serine residue of Akt was phosphorylated in Vero E6 cells in subconfluent culture and that Akt was dephosphorylated rapidly after SARS-CoV infection without up-regulation of its phosphorylation. Phosphorylation of glycogen synthase kinase-3beta, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3beta small interfering RNA indicated that the glycogen synthase kinase-3beta signaling pathway was not related to inhibition of cell proliferation. Treatment of Vero E6 cells with the phosphatidylinositol 3'-kinase/Akt inhibitor, LY294002, which induces dephosphorylation of Akt, inhibited cell proliferation. As shown in our previous studies, apoptosis occurred in virus-infected cells within 18 h postinfection. Cellular mRNA transcription, which was reported to be up-regulated in SARS-CoV-infected Caco-2 cells, was not up-regulated in virus-infected Vero E6 cells, partially as a result of apoptosis. These results suggested that inhibition of cell proliferation is regulated by both the phosphatidylinositol 3'-kinase/Akt signaling pathway and by apoptosis in SARS-CoV-infected Vero E6 cells. This is the first study to analyze SARS-CoV-induced cell growth inhibition.
DOI: 10.1111/j.1574-695X.2005.00028.x
PubMed: 16487305
Links to Exploration step
pubmed:16487305Le document en format XML
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uniqKey="Kuwabara M" first="Mikinori" last="Kuwabara">Mikinori Kuwabara</name></author><author><name sortKey="Takashima, Hideaki" sort="Takashima, Hideaki" uniqKey="Takashima H" first="Hideaki" last="Takashima">Hideaki Takashima</name></author><author><name sortKey="Yanagawa, Hiroshi" sort="Yanagawa, Hiroshi" uniqKey="Yanagawa H" first="Hiroshi" last="Yanagawa">Hiroshi Yanagawa</name></author><author><name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="RBID">pubmed:16487305</idno><idno 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last="Iizuka">Daisuke Iizuka</name></author><author><name sortKey="Inanami, Osamu" sort="Inanami, Osamu" uniqKey="Inanami O" first="Osamu" last="Inanami">Osamu Inanami</name></author><author><name sortKey="Kuwabara, Mikinori" sort="Kuwabara, Mikinori" uniqKey="Kuwabara M" first="Mikinori" last="Kuwabara">Mikinori Kuwabara</name></author><author><name sortKey="Takashima, Hideaki" sort="Takashima, Hideaki" uniqKey="Takashima H" first="Hideaki" last="Takashima">Hideaki Takashima</name></author><author><name sortKey="Yanagawa, Hiroshi" sort="Yanagawa, Hiroshi" uniqKey="Yanagawa H" first="Hiroshi" last="Yanagawa">Hiroshi Yanagawa</name></author><author><name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</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">FEMS immunology and medical microbiology</title><idno type="ISSN">0928-8244</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 Proliferation</term><term>Chlorocebus aethiops</term><term>Gene Expression Regulation</term><term>Glycogen Synthase Kinase 3 (genetics)</term><term>Glycogen Synthase Kinase 3 (metabolism)</term><term>Humans</term><term>Phosphatidylinositol 3-Kinases (genetics)</term><term>Phosphatidylinositol 3-Kinases (metabolism)</term><term>Phosphorylation</term><term>Proto-Oncogene Proteins c-akt (genetics)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>SARS Virus (pathogenicity)</term><term>Signal Transduction</term><term>Vero Cells</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glycogen Synthase Kinase 3</term><term>Proto-Oncogene Proteins c-akt</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glycogen Synthase Kinase 3</term><term>Proto-Oncogene Proteins c-akt</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Cell Proliferation</term><term>Chlorocebus aethiops</term><term>Gene Expression Regulation</term><term>Humans</term><term>Phosphorylation</term><term>Signal Transduction</term><term>Vero Cells</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is caused by SARS-coronavirus (SARS-CoV). Infection of Vero E6 cells with SARS-CoV inhibits cell proliferation. Our previous study indicated that Akt, which is poorly phosphorylated in confluent cultures of Vero E6 cells, is phosphorylated and then dephosphorylated upon infection by SARS-CoV. In the present study, we showed that a serine residue of Akt was phosphorylated in Vero E6 cells in subconfluent culture and that Akt was dephosphorylated rapidly after SARS-CoV infection without up-regulation of its phosphorylation. Phosphorylation of glycogen synthase kinase-3beta, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3beta small interfering RNA indicated that the glycogen synthase kinase-3beta signaling pathway was not related to inhibition of cell proliferation. Treatment of Vero E6 cells with the phosphatidylinositol 3'-kinase/Akt inhibitor, LY294002, which induces dephosphorylation of Akt, inhibited cell proliferation. As shown in our previous studies, apoptosis occurred in virus-infected cells within 18 h postinfection. Cellular mRNA transcription, which was reported to be up-regulated in SARS-CoV-infected Caco-2 cells, was not up-regulated in virus-infected Vero E6 cells, partially as a result of apoptosis. These results suggested that inhibition of cell proliferation is regulated by both the phosphatidylinositol 3'-kinase/Akt signaling pathway and by apoptosis in SARS-CoV-infected Vero E6 cells. This is the first study to analyze SARS-CoV-induced cell growth inhibition.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16487305</PMID><DateCompleted><Year>2006</Year><Month>05</Month><Day>10</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0928-8244</ISSN><JournalIssue CitedMedium="Print"><Volume>46</Volume><Issue>2</Issue><PubDate><Year>2006</Year><Month>Mar</Month></PubDate></JournalIssue><Title>FEMS immunology and medical microbiology</Title><ISOAbbreviation>FEMS Immunol. Med. Microbiol.</ISOAbbreviation></Journal><ArticleTitle>Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells.</ArticleTitle><Pagination><MedlinePgn>236-43</MedlinePgn></Pagination><Abstract><AbstractText>Severe acute respiratory syndrome (SARS) is caused by SARS-coronavirus (SARS-CoV). Infection of Vero E6 cells with SARS-CoV inhibits cell proliferation. Our previous study indicated that Akt, which is poorly phosphorylated in confluent cultures of Vero E6 cells, is phosphorylated and then dephosphorylated upon infection by SARS-CoV. In the present study, we showed that a serine residue of Akt was phosphorylated in Vero E6 cells in subconfluent culture and that Akt was dephosphorylated rapidly after SARS-CoV infection without up-regulation of its phosphorylation. Phosphorylation of glycogen synthase kinase-3beta, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3beta small interfering RNA indicated that the glycogen synthase kinase-3beta signaling pathway was not related to inhibition of cell proliferation. Treatment of Vero E6 cells with the phosphatidylinositol 3'-kinase/Akt inhibitor, LY294002, which induces dephosphorylation of Akt, inhibited cell proliferation. As shown in our previous studies, apoptosis occurred in virus-infected cells within 18 h postinfection. Cellular mRNA transcription, which was reported to be up-regulated in SARS-CoV-infected Caco-2 cells, was not up-regulated in virus-infected Vero E6 cells, partially as a result of apoptosis. These results suggested that inhibition of cell proliferation is regulated by both the phosphatidylinositol 3'-kinase/Akt signaling pathway and by apoptosis in SARS-CoV-infected Vero E6 cells. This is the first study to analyze SARS-CoV-induced cell growth inhibition.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mizutani</LastName><ForeName>Tetsuya</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases, 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>Iizuka</LastName><ForeName>Daisuke</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Inanami</LastName><ForeName>Osamu</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Kuwabara</LastName><ForeName>Mikinori</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Takashima</LastName><ForeName>Hideaki</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Yanagawa</LastName><ForeName>Hiroshi</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Saijo</LastName><ForeName>Masayuki</ForeName><Initials>M</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></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>FEMS Immunol Med Microbiol</MedlineTA><NlmUniqueID>9315554</NlmUniqueID><ISSNLinking>0928-8244</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.26</RegistryNumber><NameOfSubstance UI="D038362">Glycogen Synthase Kinase 3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="Y">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002522" MajorTopicYN="N">Chlorocebus aethiops</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D038362" MajorTopicYN="N">Glycogen Synthase Kinase 3</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" 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