Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells
Identifieur interne : 000509 ( PascalFrancis/Corpus ); précédent : 000508; suivant : 000510Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells
Auteurs : Tetsuya Mizutani ; Shuetsu Fukushi ; Daisuke Lizuka ; Osamu Inanami ; Mikinori Kuwabara ; Hideaki Takashima ; Hiroshi Yanagawa ; Masayuki Saijo ; Ichiro Kurane ; Shigeru MorikawaSource :
- FEMS immunology and medical microbiology [ 0928-8244 ] ; 2006.
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- Pascal (Inist)
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Abstract
Severe acute respiratory syndrome (SARS) is caused by SARS-coronavims (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-3β, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3β small interfering RNA indicated that the glycogen synthase kinase-3β 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.
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Format Inist (serveur)
| NO : | PASCAL 06-0215620 INIST |
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| ET : | Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells |
| AU : | MIZUTANI (Tetsuya); FUKUSHI (Shuetsu); LIZUKA (Daisuke); INANAMI (Osamu); KUWABARA (Mikinori); TAKASHIMA (Hideaki); YANAGAWA (Hiroshi); SAIJO (Masayuki); KURANE (Ichiro); MORIKAWA (Shigeru) |
| AF : | Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases/Tokyo/Japon (1 aut., 2 aut., 8 aut., 9 aut., 10 aut.); Laboratory of Radiation Biology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University/Sapporo/Japon (3 aut., 4 aut., 5 aut.); Department of Biosciences and Informatics, Faculty of Science and Technology, Keio University/Yokohama/Japon (6 aut., 7 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | FEMS immunology and medical microbiology; ISSN 0928-8244; Royaume-Uni; Da. 2006; Vol. 46; No. 2; Pp. 236-243; Bibl. 32 ref. |
| LA : | Anglais |
| EA : | Severe acute respiratory syndrome (SARS) is caused by SARS-coronavims (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-3β, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3β small interfering RNA indicated that the glycogen synthase kinase-3β 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. |
| CC : | 002A05 |
| FD : | Multiplication cellulaire; Apoptose; Mort cellulaire; Microbiologie; Immunologie; Syndrome respiratoire aigu sévère |
| FG : | Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie |
| ED : | Cell proliferation; Apoptosis; Cell death; Microbiology; Immunology; Severe acute respiratory syndrome |
| EG : | Respiratory disease; Viral disease; Infection; Lung disease |
| SD : | Multiplicación celular; Apoptosis; Muerte celular; Microbiología; Inmunología; Síndrome respiratorio agudo severo |
| LO : | INIST-17567B.354000142766960110 |
| ID : | 06-0215620 |
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Pascal:06-0215620Le document en format XML
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uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name><affiliation><inist:fA14 i1="01"><s1>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases</s1><s2>Tokyo</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">06-0215620</idno><date when="2006">2006</date><idno type="stanalyst">PASCAL 06-0215620 INIST</idno><idno type="RBID">Pascal:06-0215620</idno><idno type="wicri:Area/PascalFrancis/Corpus">000509</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells</title><author><name sortKey="Mizutani, Tetsuya" sort="Mizutani, Tetsuya" uniqKey="Mizutani T" first="Tetsuya" last="Mizutani">Tetsuya Mizutani</name><affiliation><inist:fA14 i1="01"><s1>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases</s1><s2>Tokyo</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Fukushi, Shuetsu" sort="Fukushi, Shuetsu" uniqKey="Fukushi S" first="Shuetsu" last="Fukushi">Shuetsu Fukushi</name><affiliation><inist:fA14 i1="01"><s1>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases</s1><s2>Tokyo</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lizuka, Daisuke" sort="Lizuka, Daisuke" uniqKey="Lizuka D" first="Daisuke" last="Lizuka">Daisuke Lizuka</name><affiliation><inist:fA14 i1="02"><s1>Laboratory of Radiation Biology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1><s2>Sapporo</s2><s3>JPN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Inanami, Osamu" sort="Inanami, Osamu" uniqKey="Inanami O" first="Osamu" last="Inanami">Osamu Inanami</name><affiliation><inist:fA14 i1="02"><s1>Laboratory of Radiation Biology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1><s2>Sapporo</s2><s3>JPN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Kuwabara, Mikinori" sort="Kuwabara, Mikinori" uniqKey="Kuwabara M" first="Mikinori" last="Kuwabara">Mikinori Kuwabara</name><affiliation><inist:fA14 i1="02"><s1>Laboratory of Radiation Biology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1><s2>Sapporo</s2><s3>JPN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Takashima, Hideaki" sort="Takashima, Hideaki" uniqKey="Takashima H" first="Hideaki" last="Takashima">Hideaki Takashima</name><affiliation><inist:fA14 i1="03"><s1>Department of Biosciences and Informatics, Faculty of Science and Technology, Keio University</s1><s2>Yokohama</s2><s3>JPN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Yanagawa, Hiroshi" sort="Yanagawa, Hiroshi" uniqKey="Yanagawa H" first="Hiroshi" last="Yanagawa">Hiroshi Yanagawa</name><affiliation><inist:fA14 i1="03"><s1>Department of Biosciences and Informatics, Faculty of Science and Technology, Keio University</s1><s2>Yokohama</s2><s3>JPN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</name><affiliation><inist:fA14 i1="01"><s1>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases</s1><s2>Tokyo</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Kurane, Ichiro" sort="Kurane, Ichiro" uniqKey="Kurane I" first="Ichiro" last="Kurane">Ichiro Kurane</name><affiliation><inist:fA14 i1="01"><s1>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases</s1><s2>Tokyo</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Morikawa, Shigeru" sort="Morikawa, Shigeru" uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name><affiliation><inist:fA14 i1="01"><s1>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases</s1><s2>Tokyo</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">FEMS immunology and medical microbiology</title><title level="j" type="abbreviated">FEMS immunol. med. microbiol.</title><idno type="ISSN">0928-8244</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">FEMS immunology and medical microbiology</title><title level="j" type="abbreviated">FEMS immunol. med. microbiol.</title><idno type="ISSN">0928-8244</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term><term>Cell death</term><term>Cell proliferation</term><term>Immunology</term><term>Microbiology</term><term>Severe acute respiratory syndrome</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Multiplication cellulaire</term><term>Apoptose</term><term>Mort cellulaire</term><term>Microbiologie</term><term>Immunologie</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is caused by SARS-coronavims (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-3β, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3β small interfering RNA indicated that the glycogen synthase kinase-3β 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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0928-8244</s0></fA01><fA03 i2="1"><s0>FEMS immunol. med. microbiol.</s0></fA03><fA05><s2>46</s2></fA05><fA06><s2>2</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells</s1></fA08><fA11 i1="01" i2="1"><s1>MIZUTANI (Tetsuya)</s1></fA11><fA11 i1="02" i2="1"><s1>FUKUSHI (Shuetsu)</s1></fA11><fA11 i1="03" i2="1"><s1>LIZUKA (Daisuke)</s1></fA11><fA11 i1="04" i2="1"><s1>INANAMI (Osamu)</s1></fA11><fA11 i1="05" i2="1"><s1>KUWABARA (Mikinori)</s1></fA11><fA11 i1="06" i2="1"><s1>TAKASHIMA (Hideaki)</s1></fA11><fA11 i1="07" i2="1"><s1>YANAGAWA (Hiroshi)</s1></fA11><fA11 i1="08" i2="1"><s1>SAIJO (Masayuki)</s1></fA11><fA11 i1="09" i2="1"><s1>KURANE (Ichiro)</s1></fA11><fA11 i1="10" i2="1"><s1>MORIKAWA (Shigeru)</s1></fA11><fA14 i1="01"><s1>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases</s1><s2>Tokyo</s2><s3>JPN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></fA14><fA14 i1="02"><s1>Laboratory of Radiation Biology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University</s1><s2>Sapporo</s2><s3>JPN</s3><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Biosciences and Informatics, Faculty of Science and Technology, Keio University</s1><s2>Yokohama</s2><s3>JPN</s3><sZ>6 aut.</sZ><sZ>7 aut.</sZ></fA14><fA20><s1>236-243</s1></fA20><fA21><s1>2006</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>17567B</s2><s5>354000142766960110</s5></fA43><fA44><s0>0000</s0><s1>© 2006 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>32 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>06-0215620</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>FEMS immunology and medical microbiology</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Severe acute respiratory syndrome (SARS) is caused by SARS-coronavims (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-3β, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3β small interfering RNA indicated that the glycogen synthase kinase-3β 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.</s0></fC01><fC02 i1="01" i2="X"><s0>002A05</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Multiplication cellulaire</s0><s5>05</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Cell proliferation</s0><s5>05</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Multiplicación celular</s0><s5>05</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Apoptose</s0><s5>06</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Apoptosis</s0><s5>06</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Apoptosis</s0><s5>06</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Mort cellulaire</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Cell death</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Muerte celular</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Microbiologie</s0><s5>08</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Microbiology</s0><s5>08</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Microbiología</s0><s5>08</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Immunologie</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Immunology</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Inmunología</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0><s2>NM</s2><s5>14</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0><s2>NM</s2><s5>14</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Síndrome respiratorio agudo severo</s0><s2>NM</s2><s5>14</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0><s5>13</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Respiratory disease</s0><s5>13</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0><s5>13</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Virose</s0></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Viral disease</s0></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Virosis</s0></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Infection</s0></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Infection</s0></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Infección</s0></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Poumon pathologie</s0><s5>16</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Lung disease</s0><s5>16</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Pulmón patología</s0><s5>16</s5></fC07><fN21><s1>135</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 06-0215620 INIST</NO><ET>Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells</ET><AU>MIZUTANI (Tetsuya); FUKUSHI (Shuetsu); LIZUKA (Daisuke); INANAMI (Osamu); KUWABARA (Mikinori); TAKASHIMA (Hideaki); YANAGAWA (Hiroshi); SAIJO (Masayuki); KURANE (Ichiro); MORIKAWA (Shigeru)</AU><AF>Special Pathogens Laboratory, Department of Virology 1, National Institute of Infectious Diseases/Tokyo/Japon (1 aut., 2 aut., 8 aut., 9 aut., 10 aut.); Laboratory of Radiation Biology, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University/Sapporo/Japon (3 aut., 4 aut., 5 aut.); Department of Biosciences and Informatics, Faculty of Science and Technology, Keio University/Yokohama/Japon (6 aut., 7 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>FEMS immunology and medical microbiology; ISSN 0928-8244; Royaume-Uni; Da. 2006; Vol. 46; No. 2; Pp. 236-243; Bibl. 32 ref.</SO><LA>Anglais</LA><EA>Severe acute respiratory syndrome (SARS) is caused by SARS-coronavims (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-3β, which is one of the downstream targets of Akt, was prevented in SARS-CoV-infected cells. However, treatment with glycogen synthase kinase-3β small interfering RNA indicated that the glycogen synthase kinase-3β 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.</EA><CC>002A05</CC><FD>Multiplication cellulaire; Apoptose; Mort cellulaire; Microbiologie; Immunologie; Syndrome respiratoire aigu sévère</FD><FG>Appareil respiratoire pathologie; Virose; Infection; Poumon pathologie</FG><ED>Cell proliferation; Apoptosis; Cell death; Microbiology; Immunology; Severe acute respiratory syndrome</ED><EG>Respiratory disease; Viral disease; Infection; Lung disease</EG><SD>Multiplicación celular; Apoptosis; Muerte celular; Microbiología; Inmunología; Síndrome respiratorio agudo severo</SD><LO>INIST-17567B.354000142766960110</LO><ID>06-0215620</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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