Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells
Identifieur interne : 000481 ( PascalFrancis/Curation ); précédent : 000480; suivant : 000482Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells
Auteurs : Tetsuya Mizutani [Japon] ; Shuetsu Fukushi [Japon] ; Daisuke Lizuka [Japon] ; Osamu Inanami [Japon] ; Mikinori Kuwabara [Japon] ; Hideaki Takashima [Japon] ; Hiroshi Yanagawa [Japon] ; Masayuki Saijo [Japon] ; Ichiro Kurane [Japon] ; Shigeru Morikawa [Japon]Source :
- FEMS immunology and medical microbiology [ 0928-8244 ] ; 2006.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Immunologie.
English descriptors
- KwdEn :
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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<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>
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<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>
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<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>
</inist>
</record>
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