Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells.
Identifieur interne : 001384 ( Ncbi/Curation ); précédent : 001383; suivant : 001385Inhibition of cell proliferation by SARS-CoV infection in Vero E6 cells.
Auteurs : Tetsuya Mizutani [Japon] ; 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.
Descripteurs français
- KwdFr :
- Animaux, Apoptose, Cellules Vero, Glycogen Synthase Kinase 3 (génétique), Glycogen Synthase Kinase 3 (métabolisme), Humains, Phosphatidylinositol 3-kinases (génétique), Phosphatidylinositol 3-kinases (métabolisme), Phosphorylation, Prolifération cellulaire, Protéines proto-oncogènes c-akt (génétique), Protéines proto-oncogènes c-akt (métabolisme), Régulation de l'expression des gènes, Transduction du signal, Virus du SRAS (pathogénicité).
- MESH :
- génétique : Glycogen Synthase Kinase 3, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt.
- métabolisme : Glycogen Synthase Kinase 3, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt.
- pathogénicité : Virus du SRAS.
- Animaux, Apoptose, Cellules Vero, Humains, Phosphorylation, Prolifération cellulaire, Régulation de l'expression des gènes, Transduction du signal.
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
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pubmed:16487305Le document en format XML
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<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>
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<term>Apoptose</term>
<term>Cellules Vero</term>
<term>Glycogen Synthase Kinase 3 (génétique)</term>
<term>Glycogen Synthase Kinase 3 (métabolisme)</term>
<term>Humains</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Phosphorylation</term>
<term>Prolifération cellulaire</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Régulation de l'expression des gènes</term>
<term>Transduction du signal</term>
<term>Virus du SRAS (pathogénicité)</term>
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<term>Proto-Oncogene Proteins c-akt</term>
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<term>Proto-Oncogene Proteins c-akt</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glycogen Synthase Kinase 3</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</term>
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<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</term>
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<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>
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<term>Apoptose</term>
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<term>Humains</term>
<term>Phosphorylation</term>
<term>Prolifération cellulaire</term>
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<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>
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